:h ; .'>'■ ^. \L LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL jw do Aavaan ivnoiivn snidiqsw do Aavaan ivnoiivn snidiosw do Aavaan ivnoiivn 3nidiq3w / Jfi_/ £ Ls -o O-V IAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL i3w do Aavaan ivnoiivn snidiosw do Aavaan ivnouvn snidiosw do Aavaan ivnoiivn snioicisw _. J\ \ A y i \ AL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL I aw do Aavaan ivnoiivn snidichw do Aavaan ivnoiivn 3Ni3ia3w jo Aavaan ivnoiivn snidiosw , -:w ■ :" AL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL L aw do Aavaan ivnoiivn snidiosw do Aavaan ivnoiivn aNmaaw do Aavaan ivnoiivn snidiqsw ffMjg M LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL L ■T- iw jo Aavaan ivnoiivn 3noici3w jo Aavaan ivnoiivn 3h\d\ EDEi5DTDD WIN 3Nnio3n jo *«»aan ivnoiivn NLM001023038 KI'jT! NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE JE NATIONAL LIBRARY OF MEDICINE <&T ^ v ,>^oT'; 3nioio3w do Aavaan ivnoiivn snidicisw do Aavaan ivnoiivn NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE if \^/\ n 3Nma3w do Aavaan ivnoiivn ^ aNniasw do Aavaan ivnoiivn 3NiDia3w do Aavaan ivnoiivn NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE aNiDiasw do Aavaan ivnoiivn SNiDiasw do Aavaan ivnoiivn snidiosw do Aavaan ivnoiivn IE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE 3NiDia3w jo Aavaan ivnoiivn 3NiDia3w jo Aavaan ivnoiivn 3nidici3w jo Aavaan ivnoiivn [#•■ I rW ^ >\A * CYCLOPAEDIA OF THS PRACTICE OF MEDICINE. Edited by Dr. H. von ZTFV^EN. PROFESSOR OF CLINICAL MEDICINE IN MLMCH, BAVARIA. VOL. VI. DISEi_\ OF THE CIRCULATORY SYSTEM, TOGETHER "WITH THE CHAPTERS ON VIIOOPING-COUGH, DISEASES OF THE LIPS AND CAVITY OF THE MOUTH, AND DISEASES OF THE SOFT PALATE. By Prof. ROSENSTEIN, of Leyden; Prof. SCHROETTER, of Vienna; Prof. LEBERT, of Vevay; Prof. QUINCKE, of Berne ; Dr. BAUER, of /^T^X Munich; Dr. STEFFEN, of Stettin; Prof. VOGEL, of / ^ ' ^ Dorpat; and Prof. WAGNER, of Leipsic. ^ranslatril is GEORGE W. BALFOUR, M.D., of Edinburgh; EDWARD G. GEOGHEGAN, M.D., of London ; THOMAS DWIGHT, M.D., of Boston; J. HAVEN EMERSON, M.D., and GEORGE G. WHEELOCK, M.D., of New York ; and J. SOLIS COHEN, M.D., of Philadelphia. ALBERT H. BUCK, M.D., New Yor^^^JM^^/^ EDITOR OF AMERICAN EDITION. NEW YORK: WILLIAM WOOD AND COMPANY, 27 GREAT JONES STREET. 1876. ( Wfc ^4 irj V '- > 10 Entered according to Act of Congress, in the year 1876, by WILLIAM WOOD & CO., In the Office of the Librarian of Congress, at Washington. \ ALL RIGHTS RESERVED. \ John F. Trow & Sox, I'RINTERS AND BOOKBINDERS, 205 to 213 East Twelfth Street, NEW YORK. BIOGRAPHICAL SKETCHES OF THE AUTHORS. Samuel Sigmttnd Rosenstein, son of the rabbi Elk an Rosenstein, was born in Berlin on the 20th of February, 1832. He received his preliminary education in the Friedrichs-Werder Gymnasium, and entered the University of Berlin in 1850. Before commencing the study of medicine, he devoted a year to the study of philology, under the direction of Bockh, Trendelenburg, and others. He passed his examina- tion for the degree of doctor of medicine in 1854, the title of his thesis being " De cyclopia inter animalia observata." Among his instructors were such men as Schoenlein, Traube, and Langenbeck. From 1856 to 1858 he acted as assistant physician in the city hospital of Dantzic. He then returned to Berlin, and continued his medical studies under Virchow and Ho2>pe-Seyler. Soon afterwards he began his career in that city as a private practitioner. In 1863 he was appointed an in- structor in the University of Berlin; in 1865 he was called to Groningen, in Holland, as professor of the medical clinic; and in 1873 he accepted a call to the University of Leyden. In addition to numerous journal articles, which appeared from time to time in Virchow's Archiv, between the years 1855 and 1873, Rosenstein has written a treatise on the " Pathology and Therapeutics of Kidney Diseases," the first edition of which was published in 1863, the second in 1869. In 1873 a translation of this work was published in the French language. Leopold Schroetter was born in Gratz, in Steiermark, on the 5th of February, 1837. His father, Anton Schroetter, the discoverer of amorphous phosphorus, was at that time professor of chemistry in the Joanacum. It was here, too, that the son received the greater part of his preliminary education, the balance of it being ob- tained in the then very nourishing Gymnasium of Vienna, under most excellent teachers. His entire course of medical studies was also completed in Vienna, his chief attention being devoted to the instruction of Schuh and Skoda. In 1861 he received the degree of doctor of medicine and surgery, and, after a service of only fifteen months in the General Hospital as a candidate for the position, he had the good fortune to be appointed a "pupil in operative surgery" in Schuh's surgical clinic, with a yearly stipend from the government. At the same time, so far as the iv BIOGRAPHICAL SKETCHES OF THE AUTHORS. duties of his position allowed him opportunity, he continued, to follow the teachings of Skoda. It was probably owing to the interest thus shown by Schroetter in his lectures, that Skoda soon afterwards chose him as his clinical assistant, a posi- tion which he held for a period of six years (from November 1, 1863, to November, 1869). Owing to Skoda's frequent illnesses, Schroetter was often called upon to conduct the clinic alone, and this increase of responsibility stimulated him to great efforts. During this period the following works were published : 1. "A Case of Recovery from Pneumothorax (in a tuberculous patient) without Pleuritic Exudation." Wochenblatt der k. k. Gesellschaft der Aerzte, No. 5, 1865. 2. " Extirpation of a Polypus of the Larynx." Wiener inedicin. Presse, No. 34, 1865. 73. " On Narrowing of the Aorta in the Vicinity of the Ductus Arteriosus Botalli." Wochenblatt der k. k. Gesellschaft der Aerzte, No. 43, 1866. ) 4. "Report of a Case of Cyst of the Epiglottis." Med. Jahrb., XII. Band, 1866. 5. " Echinococcus of the Lungs." Med. Jahrb., XIV., 1867. (This is the first observation on record of echinococcus multilocularis of the lungs.) 6. " Contributions to Laryngoscopical Surgery." Medic. Jahrb., XV., 1868. 7. " A Second Series of Contributions to Laryngoscopical Surgery." Medic. Jahr- biicher, XVI. Bd., 1868. 8. " A Third Series of Contributions to Laryngoscopical Surgery." Medic. Jahrb., XVII. Bd., 1869. 9. " On the Body Temperature observed in Croupous Pneumonia." VIII. Bd. d. Sitzuugsberichte der k. Academie der Wissenschaften, 1868. After the publication of this last^aper, he was appointed an instructor in dis- eases of the larynx and chest, in the University of Vienna. On the 4th of March, 1870, he was placed in charge of the newly-created laryngoscopical clinic, thus filling the position which Tiirck's death had for some time past left vacant. After Oppolzer's death, he was invited to take temporary charge of the first division of the medical clinic, and in 1875 he was raised to the rank of extraordinary professor. During this second period of his career, the following are among the most important of his contributions to medical literature: " Contribution to our Knowledge of the Changes in Position which the Heart may undergo." Med. Jahrbiicher, XX. Bd., 1870 ; " On the Effects of Digitalis and the Tincture of Veratrum Viride upon the Body Temperature in Croupous Pneumonia." LXII. Bd. der Sitzungsbeiielite der k. Academie der Wissenschaften. LXVI., B. III. Abth. 1872 (July number); " Laryngoscopical Communications," published by Braumuller in Vienna, 1875 ; " Contributions to the Treatment of Stenoses of the Larynx." Braumuller, Vienna, 1876 ; " On Aneurisms of the Aorta." Mittheilungen des Wiener medic. Doctoren-Collegiums, 1876, II. Bd., 12 ; " On Foreign Bodies in the Naso-pharyngeal Cavity, Larynx, and Trachea." Zeitschrift fur Ohrenheilkunde, etc., 1876. Heinrich Quincke was born in 1842, in Frankfort on the Oder. From 1858 to 1863 he studied medicine in the Universities of Wuertzburg, Heidelberg, and Ber- BIOGRAPHICAL SKETCHES OF TOE AUTHORS. V lin. In 18G6 he was made an assistant in the Bethany Hospital in Berlin, under Wilms. From 1867 to 1871 he served as an assistant in the clinic conducted by von Frerichs, in Berlin. In 1870 he established himself as a private instructor in the University of that city. In 1873 he was called to Berne, in Switzerland, as profes- sor of the medical clinic, and this position he still retains at the present day. Apart from reports of cases, he has published the following works: " On a Capillary and a Venous Pulse," Berliner klinisch. Wochenschrift, 1868; " On the Origin of the Sounds of the Heart, and on Heart Murmurs," 1870 ; " On the Treatment of Pleurisy," 1872; "On Irritation of the Vagus in the Human Being," Reichert und DuBois-Reymond's Archiv fiir Anatomic und Physiologie, 1875; " On the Excretion of Drugs through the Intestinal Mucous Membrane," 1868; "On the Influence of the Central Nervous System on the Development of Heat," (Naunyn and Quincke), 1869; "On the Circulation of Blood in the Lungs" (Quincke and Pfeiffer), 1871 ; " A Contribution to the Physiology of the Cerebro- spinal Fluid," 1872; "On Imbibition," Pfliiger's Archiv fur Physiologie, 1870; " On the Amount of Haemoglobin contained in the Blood in Different Diseases," Virchow's Archiv, 1872; " On the Length of the Period of Incubation of Typhoid Fever," Correspondenzblatt fiir Schweitzer Aerzte, 1875 ; " On Transudations con- taining Fat," Das Archiv fiir klinische Medizin, 1875 : " On Pernicious Anaemia," in Volkmann's klinischen Vortragen, 1876 ; " Balneologische Tafeln," Berlin, 1872. osef Bauer was born on the first of October, 1845, in Erlhammer, in the northern part of Bavaria. His preliminary education was obtained in part at the Gymnasium in Amberg, and in part at the Ludwigs Gymnasium in Munich. He pursued his medical studies in Munich, and in 1869 received the degree of doctor of medicine, and also the faculty prize for the best essay on " The History of Venesection." He was then appointed an assistant in the General Hospital, under the immediate direction of the late Professor Dr. Jos. von Lindwurm. In the spring of 1871 he passed the state medical examination, and devoted himself for a time to scientific researches in the laboratories. In the spring of 1873 he established him- self as a private instructor in clinical medicine in the University of Munich. He next gave courses on physical diagnosis, and also delivered lectures on certain parts of special pathology and therapeutics. After Lindwurm's death the faculty temporarily placed him in charge of the clinic, and when von Ziemssen was called to Munich (in 1874) to conduct it, Bauer still retained his connection with it as clinical assistant. In 1875 he assumed the management of the Propedeutic Clinic, established by von Ziemssen, and in 1876 he became extraordinary professor of the Propaedeutic Clinic. The following are the scientific works published by Bauer: 1. " History of Venesection," Munich, 1870. E. Gummi. 2. " On Resorption in the Small and Large Intestines." (Written in conjunction with Professor Dr. Voit.) Zeitschrift fiir Biologie, 1870. 3. "On the Transformation of Matter in Phosphorus-poisoning." Zeitschrift fiir Biologie, 1871. / VI BIOGRAPHICAL SKETCHES OF THE AUTHORS. 4. " On the Transformation of Matter after Losses of blood." Zeitschrift fiir Biologie, 1873. 5. " On the Influence of different Remedies (Quinine, Morphine, Alcohol, Digi- talis) on the Excretion of Carbonic Acid." Zeitschrift fiir Biologie, 1874 (written in conjunction with Dr. H. von Boeck). 6. " On the Results of the Cold-water Treatment in Typhoid Fever." Bayer- isches aerztliches Intelligenzblatt, 1873. 7. " On the Treatment of Croupous Pneumonia." Deutsches Archiv fiir kli- nische Medizin, 1874. 8. "On the Epidemic of Cholera in the Munich Hospital during the year 1873- 74." Bericht der Cholera Commission fiir das deutsche Reich, 1876. Dr. A. Stefpen, son of Privy Medical Counsellor Dr. Steffen, was born at Stet- tin, in the year 1825. He received his early schooling at St. Mary's High School of that city. In the autumn of 1844 he entered the University; in 1848 he obtained his degree as doctor; and in the spring of 1849 had passed the state examination. After practising medicine in Stettin from the year 1850, he became, in 1851, surgical assistant at the Children's Hospital, where, from the year 1852, he has been physician in charge. The first two volumes of his "Clinic for Children's Diseases" (diseases of the lungs and pleura) were issued between the years 1865 and 1870. His lesser works are to be found scattered through the different periodicals, and are mostly in the Jahrbuch f. Kinderheilkunde, Neue Folge. They are as follows : " On Inhalations in Tussis Convulsiva ; " " On Croup and Diphtheria of the Larynx ; " " Cases of Cerebral Tumors in Childhood ; " "On Some of the Rarer Forms of Diseases of the Brain and its Membranes ; " " Diseases of the Oesopha- gus ; " " On Tuberculosis of the Choroid and Acute Miliary Tuberculosis ; " " Con- tribution to the Study of Cardiac Diseases ; " " Contribution to the Physiology and Pathology of the Rectum ; " " On Striped Pneumonia." Alfred Vogel, son of the late Dr. August von Vogel, professor of chemistry in Munich, was born in that city, on the 31st of March, 1829. He obtained his pre- paratory education at the Gymnasium of his native city, and entered the University in 1846. In 1849 he matriculated at the University of Berlin, and followed the clinical instruction of Schoenlein, Traube, Romberg, Langenbeck, and Juengken. During the following year he visited Wuerzburg, and became an enthusiastic pupil and follower of Virchow. In the year 1851 he entered the Children's Hospital in Munich as assistant sur- geon, and in 1852 he passed his final examination for the degree of doctor of medi- cine, his thesis being on the subject of rachitis (Journal fiir Kinderkrankheiten). From 1853 to 1855 he acted as clinical assistant to Pfeufer, and while in this posi- tion he made his first steps in the career of teacher by giving courses on physical and chemical diagnosis. In 1856 he became installed as an instructor in the Uni- versity of Munich, his inaugural essay being a Treatise on Typhoid Fever (Erlan- gen, F. Encke; second edition in 1859). From this time on he conducted a very large private clinic for children's diseases. During the following years he deliv- BIOGRAPHICAL SKETCHES OF THE AUTHORS. Vli ered lectures on diseases of children, physical diagnosis, and certain portions of special pathology. In 1860 he published a Manual of Diseases of Children (Erlan- gan, F. Encke), which met with a large and rapid sale, was translated into all the principal European languages, and has now reached its seventh edition. En- couraged by a large private practice, and by the extraordinary number of patients who were brought to his public clinic, Vogel continued to devote himself to the special department which he had chosen, and added rapidly to his store of expe- rience. In 1865 he published a paper on " An Optical Test for Milk." In 1866 he was called to Dorpat, Russia, as professor of the medical clinic, a position which he holds at the present time. Since then his publications as well as those of his pupils have appeared in the " Archiv fiir klinische Medizin." Of these may be mentioned more particularly the following: " An Optical Test for Albumen;" "In- oculations with Tubercle; " " Scabies Crustosa ; " " Alterations of the Nails after Acute Diseases;" "Tetanus Rheumaticus; " "The Capabilities of the Cavity of the Mouth for Absorption; " " The ' Etat criblG' of the Cerebellum." Ernst Leberecht Wagner was born on the 12th of March, 1829, in Dehlitz, near Weissenfels, in Prussia. He received his preliminary education at the Gymnasium in Zeitz. From 1848 to 1850 he pursued his medical studies in Leipzig. The fol- lowing year he visited Vienna, where he took special delight in the teachings of Oppolzer. After remaining a year in that city, he next went to Prague, and con- tinued his medical studies in that city during the winter-semester of 1851-1852. Returning then to Leipzig, he finally, in November. 1852, passed both the state examination and that for the degree of doctor of medicine. Besides acting as private assistant to several practising physicians, he assisted Wunderlich in this capacity for a period of five years, dating from the autumn of 1853. The works on pathological histology, which were published at that time, and especially those of Virchow, excited Wagner's deepest interest, and eventually led him to accept the appointment, in 1854, of private instructor of pathological anatomy. At first he was associated with Bock in this work, but since 1854 he has been the only lecturer on this subject in the Leipzig University. In 1856 he was made extraordinary pro- fessor, and, in 1862, regular professor of general pathology and pathological anatomy. From 1853 to 1858 he also held the position of substitute prosector to the " Jacob's Hospital," but since that time he has been the regular prosector. In 1860 he was appointed director of the Medical (ambulatory) "Poliklinik." Wagner first published his works in the " Archiv fiir physiologische Heilkunde," but since 1860 he has published them in the " Archiv der Heilkunde," of which he was at that time (1860), and still is, the editor, in association with Wunderlich and Roser—formerly also with Vierordt and Griesinger. These works relate chiefly to investigations on cancer, tubercle, syphilitic new-growth, colloid metamorphosis, diphtheria, and waxy degeneration. In 1862 appeared the first edition of his " Manual of General Pathology" (published at first by Uhle and Wagner conjointly). Since then the work has been greatly enlarged, and has reached its seventh edition. The " Manual " has also recently been translated into the English language. EDITOR'S NOTE. Owing to the great size of volumes VII. and VIII., it has been deemed best to incorporate the article on Whooping-Cough, as well as those on Diseases of the Lips, Cavity of the Mouth, and Soft Palate, into this volume. CONTENTS. ROSENSTEIN. PAGH Introduction to Diseases op the Heart................................... 3 General anatomy.................................................... 7 Changes in form and position..................................... 13 Origin of sounds................................................. 18 Methods of examination.............................................. 21 Inspection...................................................... 21 Palpation....................................................... 22 Percussion...................................................... 23 Auscultation.................................................... 25 Physical symptoms of diseases of heart................................ 26 Inspection...................................................... 26 Palpation....................................................... 37 The pulse....................................................... 41 Percussion...................................................... 46 Auscultation.................................................... 48 Murmurs...................................................... 48 Their origin..................................................... 52 Their diagnosis.................................................. 54 Diseases op the Endocardium............................................. 61 History............................................................. 61 Acute Diphtheritic Endocarditis, Ulcerative Endocarditis.................... 64 Pathology........................................................... 65 Parenchymatous changes......................................... 65 Affections of other organs........................................ 69 Etiology............................................................ 70 Symptomatology................................................ 72 Diagnosis....................................................... 78 Duration....................................................... 79 Prognosis....................................................... 80 Treatment.......................................................... 80 X CONTENTS. PAGE Acute and Subacute Verrucose Endocarditis................................ 81 Pathology.......................................................... gl Position of the lesions............................. 82 Nature of the product............................................ 83 Emboli...................................... 84 Etiology............................................................ g4 Symptomatology............................... 87 Diagnosis................................. og Duration, results, and prognosis.......................... 91 Treatment................................ $% Contracting and Sclerotio Endocarditis.............................. 93 Pathology........................................................... 94 Position of the lesions......................... 94 Mode of formation............................. 95 Causes and frequency of the valvular defects........................... 98 Effects of valvular defects in general...................... 100 Insufficiency of the Mitral Valve............................... _ H9 Etiology........................................................... 119 Pathology................................................... 119 Symptomatology.......................... ■< on Course of the disease......................... 103 Diagnosis.............................................. 134 Prognosis........................................... 125 Stenosis of the Ostium Venosum Sinistrum.................. -j 25 Pathology................................................■"■"■■ ' 12g Symptomatology........................ .. „^ Diagnosis and prognosis....................... h.v. Insufficiency of the Aortic Valves....................... ' „„ Etiology................................................. " ' ^ Pathology.............................................. ' Symptomatology................................... lgg Diagnosis.............................................. ' 14Q Prognosis......................... Stenosis of the Ostium Aorticum___ * .n ....................................... 142 Pathology............................................... Symptomatology and diagnosis................... 14% Prognosis....................................... ' Insufficiency of the Tricuspid Valve. ...... „,. , , ................................... 146 Etiology and pathology.................... 1 . Symptomatology, diagnosis, and prognosis.................. 150 Stenosis of the Ostium Venosum Dextrum............. Pathology..................................................... ' i50 Symptomatology, diagnosis, and prognosis.................... 153 Insufficiency of the Pulmonary Valves.................. Etiology and pathology.......................... ' ' CONTENTS. Xi PAGE Symptomatology................................................154 Prognosis....................................................... 155 Stenosis of Ostium of Pulmonary Artery................................... 155 Etiology............................................................155 Pathology.......................................................... 156 Symptomatology................................................158 Diagnosis....................................................... 160 Prognosis.......................................................161 Combination of various Valvular and Ostial Affections......................161 Treatment of Valvular Diseases........................................... 164 Prophylaxis..................................................... 165 General hygienic rules........................................... 166 Local applications............................................... 167 Internal remedies............................................... 167 (Translated by Edward G. Geoghegan, M.D.) SCHROETTER. Changes in Position op the Heart, and Diseases op the Heart Substance 175 Normal position of the heart.............................................. 176 Turning of the heart on its axes........................................... 177 Changes in the heart's position dependent upon gravitation................... 178 Change of position by pressure............................................ 181 Changes in position occasioned by traction.................................. 183 Pathology.......................................................... 184 Diagnosis....................................................... 185 Prognosis....................................................... 186 Treatment.......................................................... 186 Hypertrophy and Dilatation of the Heart.................................. 187 History............................................................. 188 Introduction....................................................... 190 Etiology............................................................ 191 The left ventricle...................................................191 The right ventricle................................................... 196 Hypertrophy of the auricles.........................................198 Hypertrophy of the whole heart....................................... 198 Etiology............................................................198 f Dilatation of the heart.............................................. 199 Etiology............................................................ 199 Pathology.......................................................... 202 Symptomatology......................,.......................... 205 j Symptoms of dilatation..........................................212 j Diagnosis....................................................... 213 Xil CONTENTS. PAGE Course, termmation, and prognosis................................ 217 Treatment.......................................................... 218 Atronhy of the Heart.................................................... 219 history............................................................. 220 Etiology............................................................ 220 Pathology........................................................... 221 Symptomatology and diagnosis...................................222 Course, termination, and prognosis............................... 223 Treatment.......................................................... 223 Myocarditis............................................................. 223 Introduction........................................................224 ^/History............................................................. 225 Acute Myocarditis....................................................... 226 Etiology............................................................ 226 Pathology.......................................................... 228 Abscess of the heart................................................ 230 Changes in the other organs...................................... 232 Symptomatology................................................. 233 Diagnosis....................................................... 236 Course, duration, complications, and termination................... 237 Prognosis.......................................................238 Treatment.......................................................... 238 Clironic Myocarditis...................................................... 239 Etiology............................................................ 239 Pathology.........................................................240 The syphilitic form.............................................. 241 Diagnosis....................................................... 242 Course, complications, terminations, and prognosis................. 242 Treatment.......................................................... 242 Partial Aneurism of the Heart............................................ 243 Definition......................................................r 243 Acute partial aneurism............................................... 243 General description.............................................• t 243 Chronic aneurism................................................... 244 Etiology...........................................................|. 244 Symptomatology...............................................; 245 Diagnosis....................................................... 246 Treatment..........................................................' 24G Fatty/Degeneration of the Heart.........................................\ 246 IXHistory.............................................................^ 248 Etiology............................................................ 248 General description of the disease................................. , 252 Pathology.......................................................... $ -J52 Symptomatology................................................. $ >54 Diagnosis....................................................... 2 56 CONTENTS. Xiii PAGE Course, duration, and termination................................. 257 Treatment.......................................................... 259 Spontaneous Rupture of the Heart......................................... 259 History............................................................. 261 ^ Etiology............................................................ 261 Pathology.......................................................... 263 Symptomatology................................................ 265 Diagnosis and prognosis.......................................... 266 Treatment........................................................... 267 Wounds, Foreign Bodies of the Heart...................................... 267 History............................................................. 268 » Etiology............................................................ 269 Pathology.......................................................... 272 Symptomatology................................................. 275 Diagnosis...................................................... 278 Complications and terminations................................... 280 Causes of Death................................................. 281 Prognosis....................................................... 283 Treatment.......................................................... 283 New Growtlis and Parasites of the Heart................................... 284 History............................................................ 285 v Pathological anatomy................................................ 286 Fibromas and formation of concretions............................ 286 Lipomas, cysts, myomas, and carcinomas.......................... 287 Tubercle....................................................... 288 Parasites............................................................. 289 Symptomatology and course of the diseases........................ 289 Diagnosis........................................................ 290 Heart Clots............................................................. 291 History............................................................. 292 v- Etiology............................................................ 292 Pathology.......................................................... 294 Symptomatology................................................295 Diagnosis and prognosis........................................... 296 Treatment.......................................................... 297 Nervous Palpitation of the Heart.......................................... 297 History and etiology................................................. 298 ^ Pathology.......................................................... 303 Symptomatology................................................ 304 Diagnosis....................................................... 305 Course and prognosis............................................. 306 Treatment.......................................................... 306 (Translated by George G. Wheelock, M.D.) Xiv CONTENTS. LEBERT. PAGE Congenital Diseases op the Heart....................................... 311 k'History............................................................. 312 Acardia and abnormal positions.......................................314 Congenital narrowness and closure of the ostia of the right side.........314 Pathology...........................................................314 Stenosis and atresia of the pulmonary artery, with closure of the septum. 317 Stenosis of the right conus arteriosus, with an opening in the interven- tricular septum....................................................319 Simple stenosis and atresia of the pulmonary artery, with an opening in the ventricular septum............................................. 320 Combined stenosis and atresia of the pulmonary artery................322 Analysis of cases of pulmonary stenosis followed by tuberculosis of the lungs.................................................... 330 Diagnosis....................................................... 338 Prognosis...................................................... 340 Treatment.......................................................... 341 (Translated by Thomas D wight, M.D.) QUINCKE. Diseases of the Arteries, Veins, and Lymphatics.......................345 Inflammation of the External Arterial Coat, Arteritis Externa, Exartentis, Periarteritis.......................................................... 346 Pathology and course ..............................................346 Etiology...........................................................347 Symptomatology and course...................................... 348 Treatment.......................................................... 348 Periarteritis nodosa.............................................. 349 Arterio-capillary fibrosis.......................................... 350 Disease of the Middle Coat of the Arteries................................ 350 Pathology.......................................................... 351 Fatty and calcareous degeneration................................ 351 Diagnosis......................................,,................ 352 Atrophy of the middle coat.................................... 352 Hypertrophy of the media....................................... 354 Prognosis and treatment......................................... 355 Spas'in and Paralysis of the Middle Coat of the Arteries..................... 356 Etiology....................................................... .... 356 Symptomatology...............................................357 Treatment.......................................................... 361 Acute Endarteritis.......................................................362 CONTENTS. XV PAGE Pathology........................................................... 362 Etiology............................................................ 363 Symptomatology.....................»..........................365 Treatment........ .................................................365 Chroni; Endarteritis.....................................................366 Pathology........................................................... 366 Etiology.......................................................... 375 Symptomatology................................................377 Treatment.......................................................... 386 Hypertrophy of the Arterial Coats.........................................386 Pathology..........................................................387 Atrophy of the Arterial Coats............................................390 Pathology...........................................................390 Degenerations and Neoplasmata of the Arterial Walls........................ 390 Fatty degeneration.............................................. 390 Calcification.................................................... 391 Amyloid degeneration........................................... 391 Carcinoma...................................................... 392 Parasites........................................................ 393 Syphilitic Diseases of the Arteries... .f....................................394 Pathology........................................................... 394 Diagnosis and symptomatology.................................... 397 Treatment.......................................................... 398 General Dilatation of the Artenes..........................................398 Etiology............................................................ 400 Symptomatology................................................. 402 Treatment.......................................................... 404 Aneurism................•...............................................405 Pathology........................................................ 406 Etiology............................................................ 410 Symptomatology................................................ 416 Aneurism of the aorta, particularly of the thoracic aorta................417 Aneurisms of the ascending portion of the aorta.......................429 Aneurisms of the transverse portion of the arch of the aorta............432 Aneurisms of the descending thoracic aorta............................433 Aneurisms of the innominate, carotid and subclavian arteries........... 434 Aneurisms of the pulmonary artery.................................... 435 Aneurisms of the ductus Botalli....................................... 436 Aneurisms of the abdominal aorta.................................... 436 Aneurisms of other arteries in the abdomen............................439 Aneurism of the cerebral arteries.....................................440 Multiple aneurisms.................................................. 443 Diagnosis of internal aneurisms................................... 444 Course and result of aneurisms...................................447 Prognosis....................................................... 449 xvi CONTENTS. PAGE Treatment.......................................................... 449 Ligature........................................................ 4;51 Compression.................................................... 45^ Subcutaneous injection of ergotine................................ 453 Injections into the aneurismal cavity.............................. 454 Introduction of foreign bodies................................... 454 Galvano-puncture............................................... 455 General treatment............................................... 458 Internal remedies............................................... 459 Symptomatic treatment......................................... 461 Narrowing of the Arteries................................................ 463 Congenital uniform stenosis of the aorta and its branches..........464 Local contraction and obliteration of the arteries.................. 471 Contraction and obliteration of the aorta at the junction of the ductus Botalli..................................................... 473 Narrowing of the aorta in ascending portion from external pressure.. 477 Narrowing of other arteries...................................... 478 Rupture and Perforation of the Arteries. Dissecting Aneurism............... 480 Etiology........................................................... 481 Symptomatology................................................ 484 Treatment.........................................................485 Diseases op the Veins....................................................486 Acute Phlebitis...........................................................486 Pathology...........................................................486 Etiology............................... ............................487 Symptomatology...............................................488 Treatment.........................................................,489 Chronic Phlebitis........................................................ 489 Etiology...........................................................489 Pathology.......................................................... 490 Symptomatology................................................ 490 Treatment.......................................................... 491 Hypertrophy, Atrophy, Degeneration, Neojjlasms of the Venous Coats.........491 General pathology................................................... 491 Syphilitic Disease........................................................493 Pathology.......................................................... 493 Dilatation of the Veins................................................... 494 Pathology........................................................... 494 Etiology............................................................. 495 Symptomatology................................................ 496 Treatment.......................... ............................... 500 Dilatation of the Hemorrhoidal Veins___,................................. 501 Pathology...........................................................501 Etiology............................................................ 502 Symptomatology................................................504 CONTENTS. XV11 PAGE Diagnosis and prognosis.......................................... 506 1 Treatment.......................................................... 507 Diseases op the Lymphatics..............................................512 Lymphangitis, Angioleucitis............................................... 513 Pathology...........................................................514 Etiology............................................................516 Symptomatology................................................ 517 Prognosis.......................................................518 Treatment..........................................................519 Degenerations and neoplasms..............................................521 Calcification.......................................................... 521 Cancer and tubercle................................................. 521 Narrowing, Occlusion, and Dilatation..................................... 523 Etiology............................................................. 523 Pathology........................................................... 525 Symptomatology................................................. 526 Diagnosis....................................................... 528 Treatment.......................................................... 528 Narrowing and dilatation of the thoracic duct.......................... 529 Etiology.............................................................529 Symptomatology................................................. 530 Treatment ......................................................... 531 Rupture of the Lymphatics, Lymphorrhagia................................532 Rupture of the thoracic duct.......................................... 533 Composition of the lymph........................................536 Prognosis.......................................................538 Treatment..........................................................538 Chyluria............................................................ 538 Composition..................................................... 538 Etiology.............................................................539 Symptomatology................................................. 540 Nature of the disease............................................541 The filaria sanguinis hominum........................................ 542 Treatment.......................................................... 543 (Translated by George W. Balfour, M.D.) BAUER. Diseases of the Pericardium............................................. 547 History............................................................547 Absence of the Pericardium............................................... 549 Bibliography and remarks............................................ 549 Formation of Diverticuli................................................. 549 Bibliography and remarks............................................ 550 Ill CONTENTS. PAGE Tendinous Spots, Milk Spo*s.............................................. 550 Pathology........................................................... 551 Inflammation of the Pericardium......................................... 552 Pathogenesis and etiology............................................ 554 Divisions of the disease........................................... 555 Its rarity as a primary affection.................................. 555 The secondary form.............................................. 556 Influence of rheumatism.......................................... 556 Time of occurrence of the heart affection.........................557 Influence of kidney affections.................................... 557 Influence of pyamiia.............................................558 Its occurrence in the course of other diseases......... .............558 Its frequency and influence of age and sex......................... 560 Pathological anatomy................................................ 561 Stage of hyperemia............................................. 561 The fibrinous exudation..........................................561 Quantity of the fluid exudation...................................562 Formation of pus................................................ 564 Methods of progress towards cure................................. 565 Transition into chronic inflammation.............................. 566 Changes in the muscular structure of the heart..................... 567 Fatty degeneration............................................... 568 Other pathological changes....................................... 569 Symptomatology................ ............................... 570 The subjective symptoms........................................ 570 The physical signs............................................... 571 Grades of intensity of the disease................................. 572 The hemorrhagic form.......................................... 578 Chronic forms.......................................... # 579 The affection in children........................................ 5gl Inspection............................................... . 581 Palpation............................................... 533 Percussion............................................... 5gg The pericardial friction-sound...................................59I Endocardial murmurs................................ 595 Respiration..........■................................ gOl Diagnosis................................................ 007 Course, terminations, and prognosis........................ 612 Treatment................................................. 617 After-treatment and treatment of complications............. 620 Treatment by operation................................. 622 Tubercular Pericarditis......................................... 624 Pathology........................................................... 625 Symptomatology and diagnosis............................ 625 Treatment................................................. 625 CONTENTS. xix PAGE Carcinomatous Pericarditis............................................... 026 Pathology.........................................................626 Symptomatology..................................,............. 626 Adhesions between the Heart and Pericardium..............................627 Etiology............................................................ 629 Pathology..........................................................631 General description of the disease.................................635 Analysis of individual symptoms.................................. 638 Diagnosis....................................................... 646 Treatment...................................„......................649 Indurated Mediastino-pericarditis and Paradoxical Pulse..................... 649 Pneumopericardium..................................................... 657 Etiology............................................................ 658 Composition of the gas........................................... 658 Symptomatology................................................ 6C0 Diagnosis....................................................... 663 Treatment.......................................................... 663 Hydropericardium........................................................ 664 Composition of the fluid.......................................... 665 Etiology............................................................. 667 Symptomatology................................................668 Diagnosis and prognosis..........................................670 Treatment.......................................................... 671 Hwmopericardium....................................................... 671 Etiology............................................................ 671 Symptomatology................................................ 671 Free Bodies in the Pericardium........................................... 672 (Translated by George G. Wheelock, M.D.) STEFFEN. Whooping-Cough........................................................... 675 History............................................................. 679 Mode of occurrence and causation....................................683 Symptomatology and course of the disease......................... 691 The prodromal stage............ ................................ 693 The second stage................................................694 The third stage................................................. 700 Complications................................................... 701 Pathology.......................................................... 709 Diagnosis.......................................... ............ 712 Prognosis........................................................ 715 Treatment.......................................................... 719 (Translated by J. Haven Emerson, M. D. J XX CONTENTS. VOGEL. PAGE Diseases op the Lips and Cavity op the Mouth........................... 733 Herpes Labialis.......................................................... 733 Etiology........................................................... 734 Pathology......................................................... 735 Symptomatology................................................ 736 Treatment.......................................................... 738 Hypertrophy of the Lips.................................................. 738 Etiology............................................................ 739 Symptomatology ............................................... 739 Diagnosis....................................................... 740 Treatment......................................................... 741 Diseases of the Tongue ; Anatomico-histological Observations.................. 741 The muscular apparatus......................................... 742 Vascular supply................................................. 742 Nerve supply and the mucous membrane.......................... 743 Glossitis Parenchymatosa................................................. 745 Etiology............................................................ 746 Pathology........................................................747 Symptomatology................................................ 748 Diagnosis...................................................... 749 Treatment.......................................................750 Tumors of the Tongue................................................... 751 Etiology............................................................ 752 Pathology.......................................................... 752 Symptomatology................................................ 754 Diagnosis.....................................................755 Treatment....................................................... 756 Pathological Coatings of the Tongue.................................. _ 757 The manner of protrusion........................................757 Color, thickness, and extent of the coat........................... 759 Diseases of the Mucous Membrane of the Mouth............................ 762 Stomatitis Catarrhalis___......................................... _ 762 Etiology........................................................... 763 Symptomatology............................................. 764 Pathology.......................................................... 764 Treatment........................................................ 767 Difficult Dentition.....................................................77O Formation of the milk teeth.................................... 770 Symptomatology............................................... 772 Stomatitis Ulcerosa....................................................777 Stomatitis aphthosa................................................77g Putrid sore-mouth, stomacace, stomatitis mercurialis............... 782 Scorbutus of the Cavity of the Mouth....................................701 CONTENTS. XXI PAGE Etiology............,...............................................791 Pathological anatomy................................................793 Symptomatology................................................ 793 Diagnosis and prognosis.................................,........ 795 Treatment.......................................................... 796 Thrush. Fungus Formations in the Mouth................................. 797 Etiology............................................................ 798 Pathology..........................................................,800 Symptomatology................................................ 804 Diagnosis....................................................... 805 Prognosis....................,.............................. ... 806 Treatment.......................................................... 806 Gangrene of the Cheeks. Noma.......................................... 807 Etiology.......................................................... 808 Symptomatology................................................ 810 Pathology........................................................... 812 Diagnosis....................................................... 813 Treatment.......................................................... 815 Neuroses of the Mouth.................................................... 817 Sensory disturbances................................................. 818 Hyperaesthesia...................................................... 818 Anesthesia................................................. .. .....819 Anaesthesia of the nerves of taste, ageustia............................ 820 Hyperaesthesia of the nerves of taste, hypergeustia.....................821 Treatment.......................................................... 823 Motor disturbances in the mouth..................................... 823 Bulbar paralysis of the tongue........................................ 824 Treatment.......................................................... 826 Diphtheritic paralysis of the soft palate........................ ...... 826 Etiology............................................................ 826 Symptomatology.............................................. 827 Treatment.......................................................... 828 The Parotid Gland...................................................... 829 Parotitis............................................................ 830 Etiology............................................................ 831 Pathology................'.......................................... 835 Catarrh of ducts of the gland..................................... 836 Metastatic parotitis.............................................. 837 Symptomatology................................................. 839 Idiopathic parotitis.................................................. 839 Swelling of the testicles..........................................842 Diagnosis and prognosis.......................................... 846 Treatment.......................................................... 847 Ptyalis?n. Salivatio....................................................... 849 Etiology and pathogenesis............................................ 850 XX11 CONTENTS. PAGE Symptomatology......................................... ...... 852 Treatment.......................................................... 855 Deep Inflammation of the Connective Tissue of the Throat. Angina Ludovici.. 857 Etiology............................................................ 857 Pathology.......................................................... 858 Symptomatology................................................ 859 Treatment.......................................................... 860 WAGNER. Diseases op the Soft Palate............................................ 863 Anatomical remarks................................................. 863 General symptomatology........................................ .... 872 Inspection.........,............................................ 872 Palpation....................................................... 873 Local symptoms................................................. 874 Motor disturbances.................................................. 874 Sensory disturbances................................................ 876 General treatment................................................... 880 Disturbances of circulation........................................... 882 Anaemia of the soft palate.......................................882 Congestive hyperaemia of the soft palate.......................... 883 Passive hyperaemia of the soft palate.................... .........884 Hemorrhage from the soft palate................................. 884 03dema of the soft palate........................................ 886 Inflammations of the soft palate. Anginas............................ 887 Acute catarrhal inflammation of the soft palate, angina catarrhalis super - ficialis erythematosa............................................... 888 Etiology............................................................ 889 Pathology........................................................... 890 Symptomatology................................................ 893 Modifications of acute catarrhal angina............................ 895 Chronic catarrhal inflammation of the soft palate. Angina catarrhalis chronica........................................,................. 897 Etiology............................................................ 897 Pathology........................................................... 898 Symptomatology................................................ 898 Treatment........................................................ 899 The symptomatic acute catarrhal anginas..................... # 900 Angina of measles............................................ _ 900 Angina of rubeola (Rotheln—German measles)...................901 Scarlatinous catarrhal angina...................................901 Variolous angina...........................................■___902 contents. xxiii PAGE Erysipelatous angina ......................................,.....902 Herpetic angina................................................ 903 Pemphigus...................................................... 905 Phlegmonous angina................................................. 906 Inflammation of the tonsils ; amygdalitis ; angina tonsillaris............ 911 Simple or superficial catarrhal tonsillar angina................ .... 911 Lacunal catarrh of the tonsils............................,........ 912 Parenchymatous amygdalitis..................................... 913 Tonsillar abscess................................................ 914 Clinical considerations........................................... 915 Anginas which regularly appear with stomatitis........................ 921 Toxic anginas................................................... 921 Aphthous angina................................................922 Ulcerous angina................................................. 922 Angina mycotica, thrush of the palate............................923 Croupous and Diphtheritic inflammations.............................. 924 The deposit................................................... 926 Pathological anatomy................................................ 927 Clinical considerations........................................... 931 The milder forms................................................. 932 The severe forms...............................................936 The gangrenous form............................................ 945 Diphtheria of the skin........................................... 948 Diphtheritic paralyses............................................950 Scarlatinous diphtheritis........................................950 Of measles...................................................... 953 Secondary diphtheritis........................................... 953 Non-specific pharyngeal diphtheritis............................... 954 Etiology............................................................ 955 Treatment.......................................................... 960 Gangrene of the soft palate........................................... 964 Etiology............................................................ 964 Symptomatology............................................... 965 Atrophy of the palate, and especially of the tonsils.....................966 Etiology..........................................................967 Pathology........................................................... 968 Hypertrophy of the tonsils............................................ 972 Pathology.......................................................... 972 Etiology.......................................................... 974 Symptomatology................................................974 Treatment.......................................................... 977 Syphilis of the soft palate........................................... 978 Erythema..................................................... 979 Alteration of the epithelium............................ ......... 979 Papules and patches.............................................080 xxiv CONTENTS. PAGE Nodes and ulcers............................................... 981 Cicatrices.......................................................982 Treatment.......................................................... 984 Morbid growths..................................................... 984 Neoplasms of connective tissue and vessels, of fatty tissue, of muscles 985 Lymphatic morbid formations.................................... 986 Epithelial morbid formations..................................... 988 Cancer.........................................................988 Cysts..........................................................990 Nervous affections of the soft palate.................................. 990 Motor disturbances.............................................. 990 Sensory disturbances.............................,............... 993 Disturbances of nutrition......................................... 994 (Translated by J. Solis Cohen, M.D.) INTRODUCTION TO y DISEASES OF THE HEART. ROSENSTEIN. INTRODUCTION. Bibliography: Of the more easily accessible handbooks on anatomy and physiol- ogy, those of Theile-Soemmering, Luschka, Henle, Ludwig, Donders, and Funke furnish the most exhaustive information on the heart. For an exact demonstration of the relative positions of the different parts of the heart to one another and to the surrounding organs, the following illustrated works are the most impor- tant : Pirogoff, Anatome topographica sectionibus per corpus humanum trip- lici ductione ductis illustrata. Petropoli, 1852.—Luschka, Die Brustorgane des Menschen in ihrer Lage. Tubingen, 1857.—C. E Hoffmann, Die Eingeweide des Menschen, etc., 1863.—Riidinger, Topographisch-chirurgische Anatomie des Menschen. Stuttgart, 1873.—The most important monographs and essays bearing on the questions of anatomy, physiology, and physical diagnosis (the author does not aim at an exhaustive list of literature) are the following:— Harvey, Exerc. anatomicaa de motu cordis et sanguinis circulatione, etc., etc. Roterodami, 1660.—Lower, Tractatus de corde. Lugd. Batav. 1728.—J. M. Lancisi, De motu cordis et aneurysmatibus. Romas, 1728.—Alb. de Holier, Deux memoires sur le mouvement du sang. Sect. 1TI. Cap. VII. Lausanne, 1754.—Senac, Traite de la structure du cceur. Paris, 1777.—Auenbrugger, In- ventum novum ex percussione thoracis et signo pectoris morbor. deteg. Vienn. 1769; and the same, Traduite et conimentee par Corvisart. Paris, 1808.—Cor- visart, Sur les maladies et les lesions organiques du cceur. Paris, 1806.—R. La'ennec, Traite" de l'auscultation mediate. Paris, 1818, and enlarged in qua- trieme edition par Andral. Paris, 1837.—Piorry, De la percussion mediate et des signes obtenus a" l'aide de ce nouveau moyen d'exploration dans les mala- dies des organes thoraciques et abdominaux. Paris, 1827.—Rouannet, Nou- velle analyse des bruits du cceur. These, Paris, 1832.— Corrigan, On the motions and sounds of the heart, in Dublin Medic. Transac. New series, Vol. I. 1830. James Hope, Diseases of the Heart, 1830.—Bizot, Mem. de la soc. med. d'observa- tion de Toulouse. Tom. I. 1836.—Philipp, Zur Diagiiostik der Lungen und Herzkrankheiten mittelst physikalischer Zeichen. Berlin, 1836.— Corrigan, Inquiries into a new disease of the heart. Edinb. Jour. 1836. — Clendinning, Facts and inferences relative to the condition of vital organs, etc., in Med. Chir. Transact. Vol. XXI. 1838.—Beau, Recherches sur les mouvements du cceur 4 ROSENSTEIN.—DISEASES OF THE HEART. in Archiv gSner. de m6dec. 1835.—Piorry, ibid. 1834.—Bouillaud, Des Mala- dies du cceur et des grandes vaisseaux.—Reports of the London and Dublin committees for investigating, etc., in Transact, of British Scientif. Association. Vol. VI. 1837.—J. Skoda, Abhandlung iiber Auskultation und Percussion. Wien, 1839; and 5th edition, "Wien, 1854.—Gendrin, Lectures sur les maladies du cceur, 1840.—John Reid, Tables of the weights of some of the most impor- tant organs of the body, etc. Edinb. Monthly Jour, of Med. Science, 1843.— Kurschner, Herz und Herzbewegung, in Wagner's Handworterbuch, Bd. II. Oct. 1844.—Baumgarten, Ueber den Mechanismus, etc., in Mfiller's Archiv fiir Anat. und Phys. 1843.—Retzius, Ueber den Mechanismus des Zuschliessens der halbmondformigen Klappen, ibid. 1843.—J. Heine, Ueber die Mechanik der Herzkammerbewegung, etc., in Zeitschr. f. ration. Med. Bd. I. 1844.— Volk- mann, Ueber Herztone und Herzbewegung, in Zeitschr. f. rat. Medic. 1845.— Zehetmaier, Die Herzkrankheiten. Wien, 1845.—Kiwisch, Neue Theorie des Herzstosses in Prager Vierteljahrschrift, 1846, Bd. IX.—Hamernyk, Physiol. Patholo. Untersuchungen fiber den Mechanismus, etc. in Prager Vierteljahr- schrift, 1847.—Conradi, Ueber die Grosse und Lage der Brustorgane. Giessen, 1848.—Gaal, Physikalische Diagnostik. Wien, 1849.—Ludwig, Ueber den Bau und die Bewegungen der Herzventrikel, in Zeitschr. f. rat. Med. 1849.— Racle, Remarques sur certains phenomenes d'auscultation in Archiv gener. 1849.—Levie, Versuch einer neuer Erlauterung des Herzstosses in Arch. f. phys. Heilk. 1849.—Rapp, Beitrage zur Diagnostik der Klappenaffectionen des Her- zens. Habilitationsschrift. Wurzburg, 1849.— Volkmann, Die Hamodynamik nach Versuchen. Leipsig, 1850.—Kiwisch, Neue Forschungen fiber die Schall- erzeugung in den Kreislaufsorganen, in den Verhandlungen der Wiirz. phys. med. Ges. 1850.—E. H Weber, Ueber die Anwendung der Wellenlehre auf die Lehre vom Kreislauf des Blutes, etc., in Muller's Archiv, 1851.—J. Meier, Ueber die Lage der einzelnen Herzabschnitte zur Thoraxwand, etc., in Virchow's Archiv fiir path. Anat. etc. 1851 ; and Ueber die Grosse und den Grad der nor- malen Dampfung in der Pracordialgegend, ibid. Bd. III.—Traube, Practische Bemerkungen fiber den Spitzenstoss des Herzens, in Wiener med, Wochenschr. 1852.— Nega, Beitrage zur Kentniss der Function der Atrioventricularklappen des Herzens. Breslau, 1852.—Strempel, Beitrage zur physikal. Diagnostik. Habilitationsschrift. Rostock, 1852.—Knabe (Traube), De venarum pulsatione atque intumescentia Dissert, inaug. Berolini, 1853.—Scoda, Ueber die Function der Vorkammern des Herzens, in Zeitschrift der Ges. der Aerzte in Wien, 1853. —Peacock, On the weights and dimensions of the heart in health and disease, in Monthly Jour, of Med. Scie. 1854.— Wachsmuth, Ueber die Functionen der Vor- kammern des Herzens, in Zeitschrift fiir rat. Med. 1854.— W. H. Walshe A prac- tical treatise on the diseases of the lungs, heart, and aorta. London, 1854.__ Hiffelsheim, Recherches theoriques et exper. sur la cause de la locomotion du cceur, in Comptes rendus. Tom. 39, 1854.—A Heynsius, Bydrage tot eene physische verklaring van de abnormale geruischen in hel vaatstelsel, in Nederl. Lancet, 1854.-27*. Weber, Physikalische und physiologische Experimente fiber BIBLIOGRAPHY. 5 die Entstchung der Gen'iusche in den Blutgefassen, in Archiv f. physiol. Heilk. 1855.—Chauveau et Faure, Recherches experimentales sur les mouvements et les bruits du cceur, in Gaz. med. de Paris, 1855.— Vierordt, Die Lehre vom Arterien- puls in gesunden und krankhaften Zustanden, 1855.—Drasche, Ueber Verdop- plung und Spaltung der Herztone. Wiener Wochenschr. 1855.— Wulff, Non- nulla de cordis pondere ac dimensionibus, etc. Diss, inaug. Dorpat, 1856.— F. Ernst, Studien fiber die Herzthatigkeit in Virch. Arch. Bd. IX. 1856.—Bam- berger, Beitrage zur Physiol, und Pathologie des Herzens, in Virchow's Archiv. Bd. IX. 1856.— Chauveau, Sur la theorie des pulsations du cceur. Comptes rend. 1857.—Rudinger, EinBeitrag zurMechanik der Aorten- undHerzklappen. Erlangen, 1857.—Hamernyk, Das Herz und seine Bewegung. Prag, 1858.— Gerhardt, Untersuchungen fiber die Herzdampfung und die Verschiebung ihrer Grenzen bei Gesunden, im Archiv f. physiol. Heilk. 1858.—Traube, Ueber die Herz- und Arterientone in Krankheiten. Med. Centralzeitung, 1859.—Marey, Recherches sur la circulation du sang. Paris, 1859.—Spring, Memoire sur les mouvements du cceur. Mem. de l'Acad. royale de Belgique, 1860.—C. Ger- hard, Der Stand des Diaphragma, etc. Tubingen, 1860.—Schoemaker, Over hot outstaan van den ersten toon, etc. Nedel Tydschr. 1860.—Chauveau et Marey, Determination graphique des rapports de la pulsation cardiaque avec les mouve- ments de l'oreillette du ventricule. Gaz. M6d. 1861.—Beau, Traite" experimental et clinique d'auscultation, etc. Paris, 1856.—Seitz, Die Auscultation und Per- kussion der Respirationsorgane. Giessen, 1860.—Sieveking, On the diagnostic value of murmurs in the pulmonary artery. Lancet, 1860.—Ringer, On the influ- ence of change of posture on the character of endocardial murmurs. Edinb. Med. Jour. 1861.—Markham, Remarks on the cause of the closure of the valves of the heart. Med. Chir. Transact. 1861.—Sidney Ringer, On physical examination of the heart, in Edinb. Med. Jour. 1860.—Geigel, Lage und Bewegung des Her- zens, in der Wfirzb. med. Zeitschr. 1862.—Kornitzer, Anatom. plrysiol. Bemer- kungen zur Theorie des Herzschlags. Denkschrift der mathemat-naturwissen- schaftl. Klasse der Wiener Akademie, 1862.—Bahr, Zum Problem des Herzspitzenstosses. Virchow Arch. Bd. XXIII. 1862.—Scheiber, Zur Lehre vom Herztosse, ibidem.—Jacobson, Beitrage zur Hamodynamik, in Reichert u. Du Bois. Arch. 1862.—v. Dusch, Ueber ein eigenthumliches Verhalten der Herzge- rausche fur die Auscultation, in Verhandlungen des natur-histor. med. Vereins in Heidelberg, 1862.—Kobelt, Ueber Form und Dimensionen der Herzdampfung, im Archiv der Heilk. 1863.—A. von Bezold, Untersuchungen fiber die Innerva- tion des Herzens. Leipsig, 1863.—O. Naumann, Beitrage zur Lehre vom Puis. Zeitschr. fiir rat. Med. 1863, und Archiv f. Heilk. 1864.—Loeffer, Ueber Ent- stehung des zweiten Ventrikeltones. Wochenblatt der Gesell. der Aerzte, in Wien, 1862.—Scoda, Doppelter Puis und doppelte Herztone, in Allgem. Wiener med. Zeitung, 1863.—Marey, Physiologie medicale du sang. Paris, 1863.— Bamberger, Beobachtungen fiber den Venenpuls. Wiirzb. medic. Zeitschr. 1863. Geigel, Ueber den Venenpuls, ibid.— Helmholtz, Ueber Mnskelgerausch. Verhan- dlungen des medic-natur-histor. Vereins in Heidelberg, 1864.—Gerhard, Ueber 6 ROSENSTEIN.—DISEASES OF THE HEART. einige Formen der Herzdampfung in Prag. Vierteljahrschrift, 1864.—Hayden, On the rhythm of the heart's action. Dubl. Quart. Jour. 1865.—Seidel, Pulsation der Vena cava inferior bei Insuflicienz der Tricuspidalis. Deutsche Klinik, 1865.—Friedreich, Ueber den Venenpuls. Deutsche Archiv f. klin. Med. 1865. 0. J. B. Wolff, Characteristik des Arterienpulses. 1865.— C. Gerhard, Ldir- buch der Auscultation und Perkussion. Tubingen, 1866.—Donders, Der rhythmus der hartstoonen. Nederl. Arch, voar Genecsk, 1866.— Landois, Neue Bestim- mung der zeitlichen Verhaltnisse der Contraction der Vorhofe, etc. Centralblatt f. med. Wissenschaft, 1866.—Parrot, Etude clinique sur le siege et le mecan- isme des murmures cardiaques dites anemiques. Arch, gener. de medec. 1866. —Potain, Note sur les redoublements normaux des bruits de cceur. Union medic. Nos. 97, 100,104-115. 186Q.—Immermann, Zur Pathogenese und Aetio- logie der sichtbaren exspiratorischen Schwellung der Halsvenen. Deutsches Archiv fur klin. Medic. 1866.—G. Valentin, Versuch einer physiologischen Pathologie des Herzens und der Blutgefasse. 1866.—Parrot, Etude sur le siege, le mecanisme et la valeur semiologique des murmures vasculaires du cou. Arch, gener. de m6d. 1867.— Monneret, Sur les bruits veineux continus du cou. Gaz. med. de Paris, 1867.—A Leared, The sounds of the heart in their relation to pathology. Med. Times, 1867.— N. Friedreich, Krankheiten des Herzens, 2d edit. Eiiangen, 1867.—Soulier, Du frgmissement arteriel. Gazette de Lyon, 1867.—A Leared, On blood sounds. Med. Times and Gazette, 1868.—E. Leyden, Ungleichzeitige Contraction beider Ventrikel. Vir- chow Arch. 1868.—Dogiel und Ludwig, Ein neuer Versuch fiber den ersten Herzton. Berichte der mathem. physikal. Klasse der sachs. Ges. der Wissen- schaften, 1868.—v. Dusch, Th., Lehrbuch der Herzkrankheiten, 1868.—Jaccoud, Methode cardiographique de Mr. le Professeur Baccelli de Rome. Gaz. hebd. 1868.—Geigel, Der gespaltene Herzton, Verhandlungen der Wfirzburg. Ges. 1868. — 0. Bayer, Ueber die Entstehung des ersten Herzcons, etc. Arch. f. Heilk. 1869. — The Same, Casuistischer Beleg fiir die Nothwendigkeit den ersten Herzton als Muskelton aufzufassen, ibid.—Guttmann, Ueber die Entstehung des ersten Herztons. Virchow's Archiv. 1869.—The Same, Ueber den gespaltnen diastol. Herzton, etc., ibidem.—Perls, Ueber Weite und Schlussfahigkeit der Herzmfin- dungen und ihrer Klappen. Deutsches Archiv ffir klin. Med. Bd. VI. 1869.— Thamm, Beitrage zur Lehre vom Venenpuls und von den Herzgerauschen. Berl. klin Wochen. 1869.—A. B. Meier, Ueber das Hemmungsnerven system des Herzens, Berlin, 1869.—Niemeyer, P., Entwurf einer einheitlichen Theorie der Herz-, Gefass- und Lungengerausche. Deutsches Archiv f. klin. Med. 1870.— Bayer, Weitere Beitrage zur Frage fiber die Entstehung des Herztons. Archiv fiir Heilk. 1870.—Michels, Ueber die Entstehung des ersten Herztons. Diss. Berlin, 1870.—Quincke, Beitrage zur Entstehung der Herztone und Herzge- rausche. Berlin klin. Wochen. 1870.—Nolet, E. J. M., Zur Lehre der Gefass- gerausche. Arch. f. Heilk. 1871.—H. Jacobson, Ueber Herzgerausche. Berlin, klin. Woch. 1871.—Giese W., Versuche fiber die Entstehung der Herztone. Deutsche Klinik, 1871.—Silver, On functional regurgitant bruit. Med. Times and Ga- INTRODUCTION. 7 zette, 1871.—H. W. Fuller, in St. George Hosp. Reports, 1871.—Landois, L., Die Lehre vom Arteriehpuls, etc., 1872.—Paul Guttmann, Lehrbuch der klinischen Untersuchungsmethoden, etc. Berlin, 1872.—E. Hering, Ueber den Einfluss der Athmung auf den Kreislauf. Wiener acad. Sitzungsberichte, 1872.—R. Hei- denhain, Ueber arhythmische Herzthatigkeit, in Pflfiger's Arch. 1872.—Schiff, Versuche fiber die Innervation des Herzens. Reported in Centralb. f. med. Wissensch. 1872.—G. Gianuzzi, Ricerche exquite nel gabinetto difisiologie, etc., ibid. 1872.— W. R. Gowers, On the influence of posture on presystolic cardiac * murmurs. The Practitioner, 1873.—Ph. Knoll, Ueber den Einfluss des Halsmarks auf die Schlagzahl des Herzens. Wiener acad. Sitzungsber. 1873.—H Wilckens, Ueber die Rotationsbewegungen des Herzens nach einer direkten Beobachtung am lebenden Menschen. D. Arch, fiir klin. Med. Bd. XIV. 1874.—M. Jalin, Ueber Fissura sterai congenita und fiber die Herzbewegung, insbesondere den Herzstoss. Inaug. Diss. Erlangen, 1874.—Nuel, Ueber den Einfluss der Vagus- reaction aufs Herz. Pluger's Archiv, Bd. IX. 1874.—G. W. Balfour, Clinical lectures on diseases of the heart. Edinb. Med. Journ. 1874.— Talma, Beitrage zur Theorie der Herz- und Arterientone. Deutsch. Arch. f. klin. Med. Bd. XV. 1874. The heart is situated in the inferior portion of the medias- tinum, is capable of free motion, and is attached only to the large vessels. It forms an angle of 60° with the axis of the body, its base looking backwards, upwards, and to the right side, its apex forwards, downwards and to the left. Its plane side, com- posed chiefly by the left ventricle, lies on the tendinous portion of the diaphragm, while the anterior convex surface, belonging mainly to the right ventricle, together with part of the auricles, faces the thorax wall, being situated behind the sternum and right and left costal cartilages. The anterior and posterior sur- faces are separated inferiorly by the sharp border which projects into the groove formed by the diaphragm and thorax, superiorly by a rounded border, which is completely covered by the lungs. However, the anterior surface does not come in its full extent into immediate contact with the thorax, for between the two, the lungs, which surround the heart posteriorly, and over the sides, project their anterior margins. These margins meet at the level of the second rib, and run parallel to one another, down to the sternal end of the fourth rib. Here they separate, the border of the left lung bending down sharply to the left side, and forming a semi-lunar notch, the incisura cardiaca, which extends to the 8 ROSENSTEIN.—DISEASES OF THE HEART. junction of the fifth costal cartilage with the sternum, and from here again it sends a tongue-shaped process, the linguala, in- wards. This process surrounds the border of the apex, and is inserted between it and the thorax. On the size of this cardiac notch, which, even under normal conditions, is very variable, depends the extent of the heart's surface which can come into direct contact with the thorax wall; and that part alone, which comes into this direct contact, is adapted to our powers of ex- amination on the living subject. The first requisite for the objective examination of the heart in the living subject is an exact knowledge of the positions of the different parts, not only in relation to one another, but also to their surroundings. Many difficulties oppose an absolutely cer- tain determination of these positions—for instance, the presence of the respiratory contractions and expansions of the lungs, the altering condition of the diaphragm, and the varying quantity of blood in the heart itself. Still these have been overcome, and an accurate groundwork has been laid by Pirogoff and Luschka by means of sections through frozen bodies, and by Joseph Meyer, who has used Gendrin's method of puncture on the dead subject. The inquiry of most practical interest is to determine the parts which are wholly or partially covered by the lungs, to what extent they are covered, and where one should look for the vascular foramina. The following are the results of the anatomical investigations on the subject. The right auricle, of which more than half lies external to the right-hand border of the sternum, and only one-third under the bone, is one of the parts which the lungs completely cover. It extends from the middle of the sternal end of the second intercostal space to the sternal end of the cartilage of the fifth right rib. The right side of the heart, which is the main part that lies in direct contact with the anterior wall of the chest, is least covered by the lungs. Its smaller division, situated behind the sternum, reaches from the end of the third left rib to the base of the xiphoid process, while the other and larger division extends from the middle of the sternal end of the second left intercostal space to below the middle of the cartilage of the sixth left rib. Only a small segment of the left ventricle lies against the INTRODUCTION.—ANATOMY. 9 anterior wall of the thorax, the greater portion looking towards the lateral and posterior wall. The anterior segment extends from the middle of the second to the middle of the fifth left intercostal space, its exterior border corresponding with the third, fourth, and fifth left costo-chondroidal sutures. Of the left auricle the only part visible on the anterior wall of the chest is the point of the auricular appendage surrounding the pulmonary artery at the level of the second left intercostal space ; the auricle itself reaches as high as the upper margin of the second left costal cartilage, and lies quite far back behind and to the left side of the sternum, being covered by the anterior margin of both lungs, by the ascending aorta and the pulmon- ary artery. The venous foramen of the left side of the heart is situated in the second left intercostal space, and is completely covered by the lungs. The bicuspid valve lies opposite the third left rib, with its attached border projecting more or less into the second, and its unattached more or less deeply into the third intercostal space. The venous foramen of the right side of the heart lies in a line joining the sternal articulation of the fifth right rib with the lateral end of the cartilage of the first left rib. A line, drawn from the third left intercostal space close at the edge of the sternum to the sternal articulation of the fifth right rib, meets the free border of the tricuspid valve. The middle of this bor- der lies between the sternal ends of the fourth pair of ribs. The right arterial foramen is situated in the middle of the second left intercostal space, and a needle, piercing perpendicularly to the middle of the second intercostal space, about \-\ in. from the border of the sternum, will meet the semi-lunar valves of the pulmonary artery, especially the attached border of the an- terior valve. The arterial foramen of the left side lies behind the sternal articulation of the third left rib and a part of the adjoining sternum. A needle entering perpendicularly, opposite the ster- nal articulation of the third rib, a little to the left of the mid- line of the sternum, pierces the free border of the semi-lunar valves. 10 ROSENSTEIN.—DISEASES OF THE HEART. The direction of the aorta ascendens corresponds to a line drawn from the sternal end of the third left rib towards the ster- nal end of the second right intercostal space. The vena cava, too, lies directly beneath the anterior wall of the thorax, namely, external to the right sternal border, reach- ing from the middle of the first costal cartilage to the middle of the second intercostal space, or even to the sternal end of the third costal cartilage. The outer wall of the heart, as well as the commencements of the large vessels, is firmly enclosed by the pericardium, a serous sac into which the heart is reflected. The inner layer of the sac is so intimately connected with the muscular wall of the heart, that it forms, as it were, its perimysium externum ; the external layer is more or less firmly bound up with all the surrounding structures, inferiorly with the diaphragm, in front with the sternum, and laterally with the mediastinum. In addition to the mediastinum, the tendinous sterno-pericardial ligaments, supe- rior and inferior, help to connect it anteriorly, while posteriorly it is connected by loose cellular tissue with the neighboring structures, the oesophagus, the bronchi, and the bronchial glands. A layer of pavement epithelium lines the inner surface of the sac, giving to it its smooth, serous appearance. The anterior and lateral portions are covered by the pericardial pleura, but not completely, for the left costal pleura runs downwards and out- wards from the upper border of the sternal end of the fifth rib, thus not extending to the border of the sternum, while the right costal pleura runs down the sternal border as far as the sixth rib, and in this manner their edges bound a triangle of the peri- cardium (with its base looking downwards, and its apex directed upwards) which is entirely free from serous membrane. This small space, which derives its importance from its bearing on puncture of the pericardium, lies in the level of the sternal end of the fifth and sixth costal cartilages, behind them and the left border of the sternum, and has a breadth of about three centi- metres. The inner surface of both ventricles and auricles is lined by endocardium, which structure also lays the foundation of the valves by sending duplicatures into the auricles and vessels at INTRODUCTION.—ANATOMY. 11 their mouths. In order to comprehend the pathological altera- tions the endocardium undergoes, it is of importance to know that an accurate histological investigation has identified all the elements of a blood-vessel in it. The cellular tissue which con- nects the internal surface of the heart with the endocardium supplies the part of the adventitious coat, and allows the en- trance of the nerves and vessels. The layer next in order corre- sponds exactly to the media, contractile cells even having been found in it by Schweigger-Seidel; while the innermost layer with its coat of polygonal epithelium represents the intima. In the semi-lunar valves we find blood-vessels which enter the tissue at the attached margin. The prevailing view at present, in opposition to former ones, is that the auriculo-ventricular valves are sup- plied, richly supplied, with blood-vessels. The vascular supply of the anterior right nodulus of the mitral valve, of the so- called aortic nodulus, is derived from a network common to it and to the neighboring semi-lunar valves. This accounts for the frequent occurrence of disease which attacks both struc- tures simultaneously, and the fact is deserving of particular attention. The weight and dimensions of the heart have been the subject of repeated investigations, which, however, have never led to entirely harmonious results. The chief reason of this is, that the same method has not always been adopted, the heart being weighed sometimes with the auricles and part of the large ves- sels, sometimes without; even the fluid or coagulated contents have not been always previously emptied out. In measurements, especially of the thickness of the walls, particular attention should be given to the degree of rigor, and to ascertain in what phase (systole or diastole) death has occurred; further, the quantity of blood present should be noted; and one should be most careful not to include any trabeculse in the measurement. After these precautions have been taken, the normal measure to be assumed for the length and breadth of the normal adult heart (of such alone my experience allows me to speak) is between 10 and 11 centimetres. The left ventricle, from the insertion of the aorta to the apex, generally measures 10 cm. ; the right ventricle, measured from the pulmonary artery, is generally from 3 to 5 12 ROSENSTEIN.—DISEASES OF THE HEART. mm. shorter. The thickness of the wall of the left ventricle, at the level of the insertion of the mitral valve, measures from 1 to 1.5 cm., at the apex from 0.8 to 1 cm.; that of the right ventricle, at the level of the tricuspid valve, from 6 to 7 mm., at the apex 3 mm. The weight of the heart varies normally in the adult (as far as my experience goes) from 250 to 370 grammes (from 8 to Hi oz). This agrees very closely with the weighings which Blosfeld made on hearts of subjects killed by accidents, his results being an average of 346 grms. for males, and 310 grms. for females. The female heart is a little lighter than the male; with increasing age and constant length of body the weight of the heart increases, as has been demonstrated, both by measurement and weighing, by Bizot, Clendinning and Peacock. According to Clendinning's researches the weight of the heart is to the weight of the whole body as 1:158 in the male, and in the female as 1:149. Blosfeld found for males 1:178, and for females 1:153. According to Bizot's universally accepted measurements (reduced to centimetres by Dusch), the breadth of the heart in men, between the ages of 30 and 49, is 10.8 cm. and the length 9.7 cm.; in women the breadth is 9.9 and the length 9.2 cm. The circumference of the ostium venosum dextrum is 10, and that of the o.v. sinis- trum 8.5 cm., according to Luschka, who also found the ostia arteriosa dextrum and sinistrum of an equal circumference of 7 cm. My measurements, which agree with those of Peacock, esti- mate the o. a. d. as larger. Perls, in opposition to Peacock and Chevers, insisted on making a more accurate distinction between the opening proper to the heart, the ostium cardiacum, and the upper point of attachment of the semi-lunar valves, the ostium arteriosum. Carrying out this distinction for the ostia, he found that, under 40 years old, the periphery of the ostium cardiacum was on an average 6.4 mm. greater than that of the ostium arteri- osum, while after this age the relations were almost completely reversed. In the pulmonary artery a slight change towards" an equalizing of the two takes place, but never a complete reversal, as in the aorta. The averages which Perls found for the peripheries of these ostia are: INTRODUCTION. —ANATOMY. 13 Under 40. Between 40 and 50. Over 50. Ostium aorticum cardiacum................. 70.9 mm. 63.5 " 81.5 " 71.9 " 102.5 " 121 74.6 mm. 72.2 " 84.9 " 74.6 " 105.1 " 122 74.3 mm. Ostium aorticum arteriosum................. 80.1 " Ostium pulmonale cardiacum................ 85.7 " Ostium pulmonale arteriosum................ 81.3 " Periphery of the ostium venosum sinistrum 102 122.8 " Perls has also measured, by means of a special instrument, the space which the unfolded semi-lunar valves can cover, and there- by has come to the conclusion that in middle age the unfolded valves take up a greater space than that which they must actu- ally cover, while in old age they generally take up a smaller space. AVulff found, too, in the valves of the venous ostia, that the surfaces of the valves considerably outran the surfaces of the ostia, a circumstance of some weight in regard to the ques- tion of relative insufficiency. Under normal conditions, the heart is subject to both active and passive changes of position, the latter accompanying the altered posture of the body. Thus it sinks from 3 to 6 cm. to the left, or from 1.5 to 3 cm. to the right, according as the body is lying on the left or the right side. The still greater displacements, which others have observed, I can only explain, in view of my extended investigations on the subject, as exceptional cases. The heart too retreats slightly, if the sitting or upright position is ex- changed for the horizontal. This can be easily observed on the change produced in the cardiac impulse. It is self-evident that the attachment of the pericardium to the centrum tendineum must cause the heart to follow the movements of the diaphragm, which drags it down during inspiration, and raises it during ex- piration. The difference of level produced in this way in the heart's position extends to about the breadth of an intercostal space. The alteration effected by age is due to the same cause, for in young persons the diaphragm is much higher than in elderly people. All the other changes of position are active and dependent on the movements connected with the different phases of the heart's action. Auricles and ventricles contract rhythmically (systole), and dilate (diastole), both auricles and both ventricles simultane- 14 ROSENSTEIN.—DISEASES OF THE HEART. ously. The diastole follows immediately upon the systole. The periodical series of movements is as follows : Towards the end of the ventricular diastole comes the systole of the auricles, last- ing a very short time, and followed immediately by the systole of the ventricles; the ventricles then dilate, and a short pause follows, during which the whole organ rests, as both the ven- tricles and auricles are dilated—the auricles at the close, and the ventricles at the beginning of the diastole. Then follows again the contraction of the auricles, and the motion of the ventricles is repeated, in continuous regularity. During the normal fre- quency of the pulse, according to Marey's and Donders' investi- gations, the systole of the ventricles lasts f and the diastole f of the whole time. If we estimate the duration of one full series of the motions at H seconds, the systole of the auricles only lasts TV'. Marey, by means of his cardiograph, has given a very clear, graphic demonstration of both the auricular and ventricular sys- tole, in the following manner. Fig. 1. Tracing showing the relations, as regards time, between the systole of the auricles and ventricles and the cardiac impulse (from Marey). a, Commencement of auricular systole. VT, Highest point of the curve representing the b, Commencement of ventricular systole. systole of the right ventricle. 0, Highest point of the curve representing the auri- C, Highest point of the curve representing the api- cular systole. cal pulsation. INTRODUCTION.—CHANGES IN FORM AND POSITION. 15 The heart, as we shall see, changes both its form and position during each systole and diastole. The auricles undergo least change of all; their contraction beginning at the mouths of the large veins, and moving peristaltically towards the ventricular boundaries. Their longer diameter shortens, and the auricular appendages are flattened out. The ventricles, on the contrary, contract in both directions, in both length and breadth; their antero-posterior diameter alone is lengthened, and the trans- verse section of the base, which was before elliptical, is trans- formed into a circle during the systolic increase in firmness. At the same time the ventricular cone, which before occupied an oblique position, now assumes a vertical one (Ludwig). A change of position occurs simultaneously with this change of form. With each systole, the heart, as a whole, moves down- wards, and rotates from left to right on its long axis. Although this rotation was known already to Harvey, it did not become an established fact until after the observation made by Skoda and Bamberger, and particularly, in quite recent times, by Wilckens, on persons having ectopia cordis. In addition, Bamberger and Kolliker noticed in their vivisections that the large vessels also straightened themselves out. Kornitzer was the first to show that this straightening out of the spirally twisted commence- ments of the aorta and pulmonary artery is a necessary mechan- ism, to which he attributes, not only the downward movement of the heart, but also the spiral-like rotation which it performs. The phenomenon of the cardiac impulse (or, as Traube has called it, the "apical" impulse, comprehending under apical the whole of the lowermost portion of the heart) is explained by a combination of the changes of form and position just described. On the majority of healthy individuals may be observed a circum- scribed bulging of the intercostal space below and to the inner side of the nipple, between the fifth and sixth ribs (seldom be- tween the fourth and fifth), at most one inch broad, and which can be covered with the tips of two fingers. The explanation of this phenomenon has called forth a series of opinions, of which most are of merely historical interest, and do not need mention here. To this category belongs the theory pro- pounded by Kurschner, in accordance with which the heart per- 16 ROSENSTEIN.—DISEASES OF THE HEART. forms lever-like movements. Ludwig's theory rests upon a far more solid basis ; this observer maintains that, during the systolic change in shape of the heart, its base becomes circular, the apex strives to assume a position at right angles to the centre of this circular base, and in so doing it lifts itself farther away from the base. This lifting of the apex by the systolic hardening of the muscle of the heart is held by Ludwig to be the cause of the api- cal impulse. Although we must concede that this force mentioned by Ludwig contributes in a measure to the formation of the car- diac impulse, we are yet unable to harmonize his theory with many pathological conditions that come under observation—as, for example, with the absence of the apical impulse in certain valvular defects, like stenosis of the mouth of the aorta. Asa matter of fact, there are other and more important forces at work in producing this impulse, namely, first of all, the principle known in physics as the "recoil" and also the systolic change in position of the heart. Gutbrod was the first to apply the re- coil theory to the explanation of the apical impulse. According to his view, the impulse, which the inferior part of the cardiac wall receives from the blood that flows under a high pressure into the mouths of the arteries, gives rise to a movement of the apex in the opposite direction to that of the current of blood ; the pro- cess being the same as that which takes place in a Segner's (turbine) water-wheel. Hiffelsheim's experiments on gutta-percha hearts demonstrated the fact that, as regards the recoil, elastic walls behave in the same manner as those which are not elastic, and that the intensity of the recoil is directly dependent on the thickness of the wall, on the diameter of the opening through which the fluid escapes, and on the amount of the fluid. Bam- berger's objection, that the contractile force of the heart must exert against the recoil an active resistance of sufficient strength to overcome it, is thus shown to be groundless. A much more serious objection is that which Chauveau raised. This observer noticed that, in horses, the apical impulse was still perceptible after he had placed ligatures around the superior and inferior vense cavse; in other words, the impulse was still perceptible in hearts that contained, as he supposed, no blood—a fact which could not be made to harmonize with the recoil theory. M. Jahn, INTRODUCTION.—CHANGES IN FORM AND POSITION. 17 however, in repeating these experiments, found that the ligature of both venae cavae did not immediately cut off the supply of blood to the heart; on the contrary, the left ven- fig. 2. tricle continued for some little time to receive blood ■■■QH from the pulmonary veins and to drive it into the aorta. flfl No physical objections stand in the way of the application of the law of recoil to the motions of the heart. There can be no doubt, however, that the other force mentioned, i. e., the change in the I position of the heart, also contributes its influence, as Kornitzer first demonstrated. In regard to the motion of the heart downwards, and to its rotation about its long axis, as a result of the systolic I Mm straightening of the large vessels, it must be re- mm membered—as Wilckens very properly insists— I that, in the closed thoracic cavity, where the ante- rior chest wall offers some resistance to the act of rotation, this combined motion can only take place in the following modified manner: while the upper ■ part of the long axis undergoes displacement back- KM wards, the lower part approaches nearer to the wall I 189 of the chest. The apical portion will, therefore, be brought into an oblique position pointing forwards, and at the same time, owing to the downward mo- tion of the heart, it will press downwards against the tissues filling the intercostal space. Hence all the different forces—the changes in form and posi- I Bfl tion, and the recoil—mutually aid each other in producing the apical impulse. I The graphic tracing (fig 2) of the cardiac impulse shows not only the short upward stroke belonging MB to the contraction of the auricles, but also a well- marked elevation, which likewise belongs to the B beginning of the systole, and is produced by the closure of the auriculo-ventricular valves. The vibra- I tions thus produced in the valves afford an explana- tion of the tremor—observed even in healthy individ- ^^^"^* VOL. vl—2 18 ROSENSTEIN.—DISEASES OF THE HEART. uals, in whom often the apical impulse cannot be distinguished— which is confined to the region between the third and sixtli costal cartilages of the left side, and to which Traube has given the name of "valvular impulse," to distinguish it from the apical impulse. The mechanism of the closure of valves ex- plains, as Wintrich and Traube were the first to show, the origin of the sounds of the heart. On putting the ear to the apex of the heart, we at once hear two sounds, one duller, longer, and less distinct, the other higher, shorter, and more sharply defined. An extremely short interval divides the duller, longer, so-called "first sound" from the higher and shorter "second sound." A longer interval ensues between the second sound, and the following first sound; this is "the pause." Whilst the heart is in diastole, the pointed valves hang down loosely in the ventricles, in the form of a hollow cone. Owing to increasing pressure in the ventricles, to the elastic expansion of their walls, and especially to the contraction of the auricles, the points of the valves approach closer and closer to one another, till they finally touch. At the commencement of the systole the musculi papillares also contract. From each papil- lary muscle tendinous cords proceed to the different pairs of free borders (those facing each other) of the valves ; and as the points of the valves, even before the systole, were so close as to touch one another, the tension, into which the tendons are thrown during the systole, by the contraction of the papillary muscles, brings them still closer together, till the contact is firm and perfect throughout. And, further, these muscles not only prevent the valves slipping back into the auricles, but they act on them in such a manner that they (the valves) project conically into the ventricle, instead of merely lying horizontally over the opening. As soon as the chambers of the heart have emptied their contents into the large vessels, they slacken, and would allow the blood to flow back from the aorta and pulmo- nary artery, if it were not caught in the hollows of the semi- lunar valves. The sigmoid valves either lie very slack during the systole, or actually touch the walls of the vessel. But they are thrown into an increasing state of tension (with its maximum at the end of diastole) by the rising pressure of the columns of INTRODUCTION.—THE SOUNDS OF THE HEART. 19 blood on them, so that their margins come into contact, and in the shape of a three-rayed star they cut off the connection be- tween the large vessels and the ventricles. The changes in tension which both the auriculo-ventricular and the semi-lunar valves undergo in the transition from one phase of action to another (from diastole to systole, or the reverse), and the vibrations of the tense membranes thus induced, are the most important causes of the sounds of the heart; that is to say, these sounds are mainly membranous. This is almost universally admitted in the case of the shorter, clearer, and more defined second sound. Not alone that it was heard during the diastole of the heart, but the position, too, where it was best heard, over the mouths of the large vessels, rendered the connec- tion between it and the vibrations of the semi-lunar valves highly probable. But Rouanet, in 1832, was the first who experiment- ally proved that by sudden tension of the semi-lunar valves a sound was produced, and that after the destruction of these valves the second sound disappears at the mouth of the aorta. Since then the vibrations produced in the semi-lunar valves by a transition from a state of minimum tension, during systole of the heart, to a maximum tension, brought about by the pressure of the blood column on them during diastole, have been unani- mously accepted as the cause of the second sound. As might be expected, even against this explanation some raised their voices, and later Leared tried to derive the sound from the blood itself. Talma, too, has quite lately endeavored to establish Leared1 s idea on an experimental basis ; but neither Leared nor he have adduced sufficient proofs. The weak point in Talma's arguments appears to me to lie in his identifying the terms "short murmur" (kurzes Gerausch) and "sound" (Ton), although in practice we can clearly distinguish a murmur along with the sound, and the distinction can by no means be made to rest on the duration of the perception, as Talma presupposes. A murmur, however short, is still a murmur. As regards the first sound, no one any longer doubts that it is synchronous with the systole of the ventricles. But as to how it is produced, views are very much at variance. Rouanet, Bouillaud, Skoda, and Traube refer it to the vibration of the 20 ROSENSTEIN.—DISEASES OF THE HEART. auriculo-ventricular valves ; but doubt has been thrown anew on this view, already combated by Stokes and others. In Ludwig'a and Dogiel's experiments made on dogs, the first sound was still heard after every means had been taken to render the tension of the valves impossible—after all the arterial and venous trunks had been ligatured and almost all the blood expelled from the left side of the heart. This brought Ludwig once more to side with Stokes, who explained the first sound as a result of muscu- lar contraction, as a muscular sound. It is beyond all ques- tion that a muscular contraction can produce an acoustical sen- sation exactly similar to the sensory perception of the first heart sound. In a case of one-sided tetanus of the sterno-cleido-mastoid of long duration, I have had opportunity to listen to this mus- cular sound, and, by comparing it with the first sound of the heart, have convinced myself and others of the similarity of the sensory perception. Still, the supposition that the first sound is membranous is well-grounded, and conditions enough have already been given for the production of sound-giving vibrations on the auriculo-ventricular valves, in the transition from the low tension at the end of a diastole to the maximum tension during the ventricular systole. A whole series of pathological facts, collected and pointed out in this connection by Traube and Bam- berger (the explanation of which, however, would compel us to anticipate the section on pathology), are explicable exactly by assuming the first sound to be membranous. There appears to be so little connection between disease of the cardiac muscle and the intensity of the first sound in the different cases, that from a clinical point of view it is impossible to regard this as a mere muscular sound. In regard to the genesis of this first sound, we may surely consider the contraction of the wall of the ven- tricle as auxiliary, and in the same category may be placed the vibrations of the tendinous cords, but we should not regard it as a pure muscular sound. The explanation of the longer duration of the first sound, in contradistinction to the second sound, may, perhaps, be found in this prolonged vibration of the papillary tendons, while, on the other hand, the semi-lunar valves are thrown into vibration only at the moment of their closure, and are immediately restored to equilibrium by the INTRODUCTION.—METHODS OF EXAMINATION. 21 pressure of the blood. We cannot consider Talma's attempt to explain the first sound as a blood murmur as more for- tunate than his similar interpretation of the second sound. In the large vessels near the heart, too, we still hear two sounds, the second of which has its origin at the mouths of the arteries, and is transmitted along them. But the first sound is by no means to be considered as the transmitted first sound of the heart, as it is still to be heard after the first heart sound has become inaudible or has been replaced by a murmur. The first vascular sound is also membranous, and is produced by the vibrations excited in the walls of the vessels by the sudden increase of tension due to the systole of the ventricles. Although Talma's interpretation of this first vas- cular sound as a blood murmur has here much more appearance of probability, still I cannot yet regard it as proved. It is better in the meantime to hold to the view that we can distinguish six different sounds, according to the manner of their origin—two which owe their existence chiefly to the vibrations of the auriculo- ventricular valves, two to the vibrations of the semi-lunar, and two to the vibrations of the walls of the large vessels. Methods of Examination. The methods which we adopt to ascertain the symptoms of the normal condition of the heart, or the variations therefrom in case of disease, consist in inspection, palpation, percussion, and auscultation. The following are the results given by the sev- eral methods for the normal condition: Inspection of the left thoracical region shows no difference between it and the right side, either in regard to the arch- ing of the wall or the thickness of the layers of skin and muscle. But in the majority of healthy people we perceive a rhythmically occurring protrusion of the fifth, seldom of the fourth, intercostal space, exactly between the mammillary and parasternal lines, internal to and below the nipple, with a maximum breadth of one inch, and two finger-tips deep. This phenomenon, the visible impulse of the heart, may be absent even in quite healthy people, if the soft parts overlying it 22 ROSENSTEIN.—DISEASES OF THE HEART. are too thick, or if the lung be abnormally spread over the heart; finally, if the apex beat behind a rib. The time of life, too, exerts quite normally a great influence on the position of the impulse, due to the situation of the diaphragm—in young children rendering it perceptible higher up, but still within the mammary line, though not unfrequently external to the nipple (in one case I saw it 3 cm. outside), while in old people it is to be seen lower down. The posture of the person to be examined also alters the position of the impulse in hearts which are other- wise quite normal. As the heart is movable to either side, when the body lies on the left side, we see the impulse move towards the left, and towards the right if the body lie on the right. The motion towards the right is more restricted, but still quite discernible. When its action is excited we see the movement of the heart in several intercostal spaces, and often, especially in lean individuals, a movement traversing the whole region from above and the right, towards below and to the left. The place the wave has just passed sinks for an instant, while the next part rises. Along the left border of the sternum we can observe that the third, fourth, and more rarely the fifth, intercostal spaces sink synchronously with the cardiac impulse, though this be quite in its normal position. The explanation Friedreich offers, that the parts of the heart which lie along the sternum assume a smaller volume than the rest, is founded on an arbi- trary assumption, and is even more unsatisfactory than Bam- berger's theory, according to which the intercostal spaces, over which the heart has just passed from above downwards with greater rapidity, yield to the atmospheric pressure, and conse- quently fall in. In palpation, the finger is laid over the region of the heart, and experiences a slight elevation. It is impossible to describe the normal degree of resistance, a matter which can alone be learned by practice. One must not forget, however, that the force of the impulse varies according to the degree in which the lung covers the apex of the heart, according as the patient breathes lightly or heavily, according as he is calm or excited, so that every variation from the normal is not to be regarded immediately as pathological. Palpation is not only of use in estimating the INTRODUCTION.—METHODS OF EXAMINATION. 23 resistance of the impulse, but serves also as a means of confirm- ing as pulsatory the movements on the anterior surface of the thorax and in the neck, which give the eye an impression of pul- sation, and of thus distinguishing apparent from real pulsations. The palpation of the pulse will be specially treated along with the consideration of phenomena dependent on the vessels. By means of percussion we can mark out the boundaries of the anterior portion of the heart, which lies against the thorax wall — either the part uncovered by the lungs, or the whole. The former of these gives a perfectly dead, the latter only a dulled percussion sound. Thus we can distinguish over the heart a region of absolute dulness and one of relative dulness ("Herz- mattheit," and "Herzdampfung"), or, to use the English termi- nology, superficial and deep-seated dulness. The best mode of percussing is writh the fingers, which can be adapted to each intercostal space, and at the same time they can estimate the resistance of the part percussed, thus combining palpation and percussion. If a plessimeter be used, the best form is a vulcanized india-rubber one (that of Seitz), the narrow part of which will fit into an intercostal space. The individual under examination must lie on his back, or sit upright. On account of the above-mentioned displacement caused by lying on the side, this posture must be avoided. The percussion must be light or heavy, according as we wish to hear the superficial or the deep-seated dulness. Where the lung covers the heart strong percussion is necessary to render the dulness of the un- derlying parts audible ; while by light percussion, where the heart is uncovered, we avoid disturbing the equilibrium of the adjacent pneumatic parts. Although the estimation of this rela- tive dulness undoubtedly possesses great value, yet it cannot be concealed that the absolutely accurate determination of the boundaries, superiorly and to the right side, is an impossibility, and that the manifold transitions from one degree of dulness into another can only be recognized by the most practised ear, and that consequently by this method, using all possible precau- tions and care, we can only attain to an approximate estimate of the size of the heart. Hence determination of the extent of abso- lute dulness is sufficient for all practical purposes, since, moreover, 24 ROSENSTEIN.—DISEASES OF THE HEART. all alterations in the extent of the whole heart are attended with proportionate alterations in the extent of the parts uncovered by the lungs. Thus one should always endeavor to obtain the boun- daries of the region of relative dulness of the heart; but when it is a matter of hasty general diagnosis, it is better to begin at once with the extent of the absolute dulness, and rest content with this. The best method of finding this latter, is to begin by noting where the apical impulse is visible or palpable. By this means we get the left inferior boundary. Next we find the upper limit by percussing down along the left margin of the sternum. Starting from the left mammillary line, we can then determine exactly the breadth of the dulness, and draw the left boundary line. Over the sternum itself, we get no absolutely dull sound, though the heart lies directly under its lower end. Since the left lobe of the liver is only separated from the sharp inferior border of the heart by the diaphragm, we cannot directly estimate the full extent of the inferior boundary of the area of absolute cardiac dulness. But still we ascertain a part of its cir- cumference, or, as the case may be, of its end, by means of the tym- panitic sound of the stomach, where it is sharply divided from the loud lung sound, on the left side; and from the right, by prolong- ing the line which divides this loud lung sound from the absolute dulness of the liver. If the resulting outline figure of the area of absolute cardiac dulness be projected on the breast, we obtain a triangle in most cases ; less frequently, an irregular quadrilat- eral, when the anterior border of the left lung has more than one curve, thus making the boundary line appear as if bent at an angle. This triangle is so placed that its apex coincides with the junction of the fourth left rib and sternum, its right side runs parallel to the left border of the sternum as far as the sixth rib, and its basis corresponds to the upper border of the sixth rib, while its left border runs either in an outwardly convex curve, cutting the fifth rib, or almost in a straight line down to the point of the impulse, forming, as it were, the hypothenuse of an almost right-angled triangle. The height of the triangle is from 5 to 7 cm., and its greatest breadth from 6 to 8 cm. The area of relative cardiac dulness sometimes begins as high up as the second intercostal space, especially in childhood, when INTRODUCTION.—METHODS OF EXAMINATION. 25 we can see and feel the heart's impulse between the fourth and fifth ribs ; it is always present in the third intercostal space, and measures from 2.5 to 6.5 cm. in breadth, for it extends as far as the middle line of the sternum. In the fifth space, on the right side, the dull percussion sound can be plainly heard over the inferior part of the sternum, which borders on the xiphoid process, and about two centimetres beyond the right sternal margin. The total breadth of the dulness at this level is from 8 to 13 cm. Kobelt has shown that the area of cardiac dulness is dependent on the age of the individual and the circumference of the thorax, but not on the total length of the body. If we compare the boundaries of the area of absolute cardiac dulness with those of the area of relative dulness, we shall find that a girdle of dulness, weaker above and to the right, more in- tense to the left, spreads itself around the triangle of superficial dulness. This is so distributed, that if we project it on the tho- rax, a cone is produced with its blunt apex generally in the third intercostal space, near the left margin of the sternum, its right boundary generally keeping close to the right sternal mar- gin in the fourth space, and in the fifth passing slightly beyond it; its limit to the left generally remains inside the mammillary line, while a line which unites the superior limits of the liver with the point of the heart's impulse forms its base. In auscultation, which is best executed with the stethoscope, we hear two sounds, as already explained. It only remains to point out where the sounds of the different ostia are to be best heard. From the detailed account of their relative positions, which we have given in a former paragraph, it is clear that they lie within a narrowly bounded space, alongside, sometimes even behind, one another; and moreover that they are all of them more or less covered by the lungs, and so it is only possible to auscultate the sounds of the pulmonary artery and tricuspid valve directly above where they originate, and even then but approximately. Thus, too, we auscultate the sounds produced by the mitral, not at the point corresponding to this valve, but in the region of the apex ; that of the tricuspid on the right border of, and over, the sternum at the level of the fifth rib ; the sounds of the aorta are to be sought by following the course of the ascending 26 ROSENSTEIN.—DISEASES OF THE HEART. branch, on the right margin of the sternum, between the second and third ribs, and not where they are produced by its semi-lunar valves behind those of the pulmonary artery; the sounds of the pulmonary artery are best heard in the second left intercostal space close to the border of the sternum. In the majority of healthy people the sounds of the auriculo-ventricular valves beat in the trochaic rhythm, with the accent on the first (—^), while the sounds of the semi-lunar valves of the large vessels follow the iambic metre, with the accent on the second (^ —). But it is not necessarily a sign of disease to hear the pointed valves beating in iambic measure. Physical Symptoms of the Diseases of the Heart. The same methods which enlighten us on the normal con- ditions of the heart also afford us the symptoms of its patho- logical bearing. , First: Inspection makes us aware of the abnormalities of the anterior walls of the thorax. If the volume of the heart is increased to a considerable degree, or the pericardium extensively swelled by an abundant exudation into its cavity, we may notice a protrusion of the region of the left breast, which lies over the heart, i. e., the part between the left margin of the sternum and the left nipple, from the third rib down to the seventh; this occurs most frequently in youth while the chest is still flexible. The abnormal protrusion can extend in exceptional cases, particularly in large pericardial exudations, as far as the sternum, and beyond to the right side, thus compelling the retreating left lung to withdraw completely to the upper part of the thorax. This protrusion (voussure of French authors) is not to be confounded with asymmetry of the thorax arising from other causes, and especially with the protrusion of the left side due to curvature of the spine, more particularly the form of skoliosis, where the middle dorsal vertebrae are convexly curved to the left. It is only in cases of extraordinarily large pericar- dial exudations that we find the intercostal spaces themselves projecting convexly forward. Inspection affords us other important symptoms in regard to INTRODUCTION.—PHYSICAL SYMPTOMS. 27 the changes in the apical impulse. This can either be completely wanting, or can occur at an abnormal point, or exhibit itself over a greater surface. We have already learned to account for its absence under normal circumstances ; for example, owing to an extraordinarily thick coat of soft parts on the wall of the thorax, very narrow intercostal spaces, or abnormal condition of the incisura cardiaca of the left lung, especially enlargement of the lingula. Amongst the pathological causes we may reckon : a, emphysema of the left lung; b, abundant secretion of an elastic or oily fluid in the pericardium ; c, adhesion of the heart to the surrounding pericardium ; d, certain valvular defects, such as stenosis of the ostium aortae and stenosis of the ostium venosum sinistrum, if they are well marked. The cardiac impulse is seen in other than normal conditions (always, of course, provided that the individual to be examined is made to lie on his back, since, as before stated, if he lies on one side, the impulse falls to that side)— 1. To the left of the mammillary line, extending an unusual distance in that direction, even as far as the anterior axillary line. The necessary conditions for producing this are : either, a, horizontal position of the heart, due to abnormal elevation of the diaphragm, without regard to the causes that may have produced this elevation ; or, b, abnormal increase in size and bulk of the muscle of the heart from valvular defects ; or, c, dis- placement to the left, whether it be owing to abnormal pressure on the mediastinum through a collection of elastic or oily fluid, or a tumor in the right pleura, or a vacuum caused by the shrink- ing of the left lung. Right-sided pleural exudations generally cause a dislocation of the liver rather than of the heart. 2. Outside the mammillary line to the right. The impulse of the heart may be seen on the right border of the sternum between the third and fifth ribs, corresponding in this case, however, to a section of the base of the heart, not to the apex. This is brought about by dislocation of the heart produced through an accumulation of elastic or oily fluid in the left pleura. The pulsation we see on the right side is rarely to be attributed to the apex, for the heart in its dislocations does not alter its par- allels. It is only in congenital transposition of the viscera that 28 EOSENSTEIN.—DISEASES OF THE HEART. the entire heart, including the apex, may be seen occupying the right half of the chest; this, however, is an occurrence of great rarity. In a case of contraction of the right lung and vicarious enlargement of the left, I found after death the heart displaced to the right, but in an almost vertical position, with the apex looking straight down, below the sternum. The pulsation of the part which lay furthest to the right was to be seen close to the right border of the sternum between the fourth and fifth ribs. 3. The impulse of the heart is seen lower down, between the sixth and seventh, or seventh and eighth ribs. This deep situated impulse is at the same time usually located to the left of the mammillary line, and happens in cases of decided increase in size of the left heart, due to valvular disease—for example, dis- ease of the aortic valves. Frequently we merely find a deep- situated impulse, but not outside the mammillary line. This is especially the case in those enlargements of the heart which originate in an abnormal resistance in the peripheral circulation, such as atrophy of the kidneys and sclerosis of the aortic system. 4. The impulse of the heart may be found higher up, be- tween the fourth and fifth ribs, or even between the third and fourth ribs, especially in children. This form, too, usually oc- curs outside the mammillary line. The cause is the abnormal elevation of the diaphragm, which in one series of cases is pushed up by ascites, meteorismus, upward dislocation of the left lobe of the liver, or tumors ; in others it is drawn up by contraction of the left lung, or, finally, it may assume a higher position, owing to strongly developed kyphosis, or kyphoscoliosis. The kyphosis must have attained to very large dimensions in order to be considered the cause of this displacement; for the great majority of kyphotic cases do not affect the position of the impulse at all. Pregnancy, too, although at this period the dia- phragm is raised, still seldom elevates the heart's impulse. I cannot concur with Walshe's opinion that pericarditis ever causes upward displacement. 5. The majority of cases of displacement of the cardiac im- pulse is accompanied by an alteration in the size of the surface over which it extends. When hypertrophy is the cause of downward displacement, or when the heart, even without under- INTRODUCTION.—PHYSICAL SYMPTOMS. 29 going hypertrophy, comes in direct contact with a larger surface of the thorax wall, the impulse is visible in several intercostal spaces, and increases considerably in volume—in a word, it be- comes diffuse. The intensity of the diffuse vibration is directly proportional to the amount of hypertrophy. Dilatation and hypertrophy of the right ventricle can displace the pulsation far to the right; in one case, which came under my notice, it lay 8 cm. beyond the right margin of the sternum. Instead of the protrusion, which is the normal result of the impulse of the heart, a retraction can sometimes be perceived synchronously with each systole, and in some cases extending to the inferior portion of the sternum and the ribs attached to it. Only such retractions as are confined to the point of apical im- pulse (and not till this point has been defined by percussion), whether they extend to the sternum or not, are of any diagnostical value ; while retractions of intercostal spaces (which the begin- ner must not confound with those due to respiration) in the vicinity of the impulse, whether this be present in its normal position or absent, have no significance, and belong to the large class of normal phenomena. If, for instance, the apex beat be- hind a rib, we very frequently see a contraction of the next up- per space. Skoda was the first to point out that simultaneous adhesions between the two folds of pericardium, and between the pericardial and costal pleurae, are the causes of this phenomenon. However, it is easy to convince one's self, that obliteration of the pericardium can occur without any appearance of this systolic contraction ; and, on the other hand, Traube has demonstrated that a single cord of connective tissue between the heart and pericardium is alone sufficient to produce this symptom. Again, I myself have found a stringy adhesion between the anterior parts of the visceral and parietal pericardia on making the post- mortem examination, where during life there was no trace of a systolic retraction. From this many-sided evidence we may con- clude that it would be a great mistake to assume an extended obliteration of the pericardium on the ground of a systolic retraction which was confined to the region of the apical impulse. This diagnosis can only be established with certainty when a systolic retraction of the lower portion of the sternum, along 30 ROSENSTEIN.—DISEASES OF THE HEART. with the left inferior costal cartilages, and a diastolic recoil of these parts take place. Friedreich first pointed out the con- ditions of this sum of symptoms, and properly assigned, as the main cause, the firm adhesion of the inferior surface of the heart with the diaphragm, accompanied by strong action of the heart; for the diaphragm is drawn up by the systolic shortening of the heart, and consequently it draws inwards those parts of the thorax which correspond with its own insertions. Besides the abnormal variations already described, we may meet pulsations which are quite unconnected with the apex, and originate in the right side of the heart, or proceed from the large vessels. When, for instance, the diaphragm is unnaturally sunken, a pulsation is usually visible on the border of the left arch of the ribs, exactly isochronous with the apical impulse. It moves downwards and inwards during a deep inspiration, but never crosses to the right of the middle line. This pulsation is des- ignated in general terms "epigastric," and indeed a narrow strip of the epigastric space does pulsate. But still, to avoid confusion with another form, which occurs uniformly right in the middle of the epigastrium, it is better to designate the first-mentioned as "parepigastric." This proceeds from the right ventricle, which, when the diaphragm sinks, assumes a more horizontal position, and projects its sharp border into the groove between the ante- rior thorax wall and the diaphragm. The fact that in auscul- tation we hear both cardiac sounds over the pulsating part with the same intensity as over the rest of the heart, and that pal- pation proves this and the apical impulse to be isochronous, renders the origin from the heart a certainty ; in addition, we can in some cases even feel the very muscular hardening. The presence of this pulsation proves nothing but the sunken position of the diaphragm. Where the lungs are large, it may occur (in Holland, for instance, where the lungs are mostly very large, it is of almost universal occurrence) without the presence of the slightest change in the heart, especially in the volume of this organ. Hypertrophy of the right side of the heart, how- ever, can increase the sunken condition of the diaphragm, by increasing the weight, and in this light the above-mentioned pul- INTRODUCTION.—PHYSICAL SYMPTOMS. 31 sation may in many cases be regarded as a symptom of right- sided hypertrophy of the heart. The strictly epigastric pulsation has an altogether different signification. It is the result either of increased innervation of the abdominal aorta or coeliac artery, or else of the improved con- duction of the normal pulsations of these vessels. This latter is caused by an increased firmness of the overlying solid parts, whether it be due to a hypertrophied liver, or to the presence of some abnormal tumor springing from the stomach, the retro- peritoneum, or any other structure in the epigastrium. Over this pulsation we can only auscultate one sound. When the liver itself "pulsates" (as in the case of a regurgi- tation into the hepatic veins, due to tricuspid insufficiency), and does not merely conduct the pulsations of the underlying vessels, then the phenomenon is not confined to the epigastrium ; on the contrary it is generally observable over the whole extent of the liver, more especially to the right of the middle line. Other pulsations connected with the diagnosis of heart dis- eases can be perceived on the large trunks of the aorta and pul- monary artery, also on the jugular and other cervical vessels. In exceedingly rare cases, and when the subjects are very ema- ciated, pulsation may be observed in the second intercostal space, close to the right border of the sternum. This can occur under otherwise perfectly normal conditions; it is isochronous with the heart's impulse, and originates in the aorta ascendens. Another visible and palpable pulsation, generally extending over the two first intercostal spaces and likewise close to the right border of the sternum, is due to a dilatation of the aorta ascen- dens. This dilatation is either connected with an insufficiency of the aortic valves, or occurs as an independent disease of this vessel. Of more frequent occurrence is a circumscribed pulsation aris- ing from the pulmonary artery, and exhibiting itself one or two centimetres from the left border of the sternum, and also, like the others, in the second intercostal space. From palpation we learn that the stroke occurs in synchronism with the diastole of the heart. If this pulsation corresponds to the normal position of the pulmonary artery, it must be accounted for either by an 32 ROSENSTEIN.—DISEASES OF THE HEART. abnormally thin thorax, or by a layer of solid parts, such as pul- monary tissue or tumors, which serve to transmit the impulse better. If the pulsation is further removed from the border, say three or four centimetres (the distance varies as the heart has been more or less displaced to the left), it must be regarded as a pathognomonic symptom of contraction of the left lung. We often observe pulsations of the jugulum when the heart's action is merely excited, but not otherwise altered; and these are especially frequent when the aortic arch lies high up. There is no special signification attached to this, unless it occurs when the individual under examination is perfectly at rest, and unless we can feel it. Under these conditions it points either to an anatomical anomaly (as such I have seen it twice, in the form of a longer and more tortuous arteria innommata than usual), or, as is more usual, it points to dilatation of the aortic arch, which occurs either in connection with insufficiency of the valves of the aorta, or occurs primarily as an aneurism. Constant pulsations in the large cervical arteries, the carotids, is only visible when the action of the heart is considerably increased; while neither the large internal and external jugular veins, nor the small subcutanea colli or thyroidea, etc., are ever visible except when they shine through a very soft skin, as we meet it in some women and children. Consequently we can diag- nosticate anomalies in the movements of the contents of the cer- vical veins (especially of the internal jugular, which usually runs down along the posterior border of the sterno-mastoid), if we see them projecting prominently in an over-filled con- dition. These anomalies consist in obstructions to the flow of blood towards the right side of the heart, which may be caused by general mechanical difficulties, such as diminished driving power of the heart, diminution of the elasticity of the lungs, and other forces which would tend to raise the pressure on the intrathoracic venous trunks ; it can also happen that the obstructions are of a more local nature, such as mediastinal tu- mors, which directly prevent the veins from emptying them- selves. A closer examination is then necessary to establish the special hindrance. While an abnormal dilatation is only a general sign of existing disease, which may arise from the most&widely INTRODUCTION.—PHYSICAL SYMPTOMS. 33 different causes; on the contrary, a movement in the cer- vical veins, perceptible both to sight and touch—in a word, a pulsatory movement—has a much more specific signification. This pulsatory character is of the most decisive importance, and the first precaution we must take is to see if the motion does not consist of a mere swelling which occurs with every increase of the intra-thoracical pressure {i.e., during expiration)—we must, in fact, make certain that it is not connected with respira- tion. To exclude respiratory influence alone, is, however, not enough, since movements, which are synchronous with the heart's movements, may be visible in the veins of the neck, without being thereby real pulsations. Every sharp systole of the auricle can by its retreating waves set the contents of the over- filled veins in vibration, and produce undulations in them. And, on the other hand, for a certain diagnosis' it is not sufficient to establish merely a pulsating character in general, since a vein, especially the internal jugular, owing to its close relations with the carotid, can exhibit a pulsation which has only been transmitted to it from the artery. Consequently, to estab- lish the venous pulsation as such, and as originally and directly produced by the heart, we must shut out all the possibilities of error mentioned. To effect this, it is only necessary to com- press the vein, and thus temporarily cut off the peripheral sup- ply. If the cause of the pulsation be a central one, and if it be not a mere vibration of the over-filled vein, the part beyond the compression ought to continue pulsating, since this peripheral compression has no influence on the auricle and right ventricle. If it was merely undulation, the motion would now cease; if it lay in the pulsations of the adjacent artery, it will be visible above the compression, where the vein is still full, and will cease to appear below, where the vein is empty. It is clear that compression of the carotid would be alone sufficient to decide this point; but it is not always easy to remove the full vein from the artery. This phenomenon of pulsations, which is to be seen both in the large and small cer- vical and facial veins, was known already to Allan Burns. The investigations of Geigel, von Bamberger and Friedreich, after a lively discussion of the subject, have set it now beyond all ques- VOL. VL—3 34 ROSENSTEIN.—DISEASES OF THE HEART. tion. The first condition necessary for the production of a blood- wave running from the heart to the jugular veins, is inability of the venous valves to close. These valves normally hinder re- gurgitation, and where this insufficiency does not exist, no venous pulse is visible. The closure of these valves, and of the circular muscles of the right auricle, is the cause which prevents us from seeing and feeling retreating waves at every auricular systole. While this barrier remains intact, no retreating wave, in whatever way it may be produced, can pass out beyond the sinus venosus. Thus the venous pulse can be produced through insufficiency of the jugular valves alone, however this latter may have come about, whether through anatomical or functional changes ; and the direct diagnostic conclusion we are compelled to draw is necessarily insufficiency of the venous valves. But it is self-evident that the venous pulse produced by this defect will be more distinct and intense the larger the retreating wave is, and the greater the force with which it is driven into the veins. These conditions are most completely fulfilled by a defect in the closure of the tricuspid valve, when, with every systole, a portion of the blood, instead of being directed from the heart into the pulmonary artery, is driven by the force of the ventricle into the right auricle, the venae cava and innominata, and past these out into the cervical veins. But even against the force of the regur- gitation, which accompanies tricuspid insufficiency, the venous valves can remain a long time closed. So in some cases this defect of the tricuspid can occur without causing a cervical venous pulsation, and, on the other hand, a most pronounced venous pulse can occur without defect of the tricuspid. This latter may be the result of frequent stagnation of the circulation, due to long fits of coughing (as in bronchial catarrh), affecting the closing power of the valves ; or it may be an unclosed fora- men ovale, accompanied by insufficiency of the mitral valve, as in Reisch's celebrated case: and thus with every systole a large quantity of blood is driven through the left auricle into the right auricle. I have observed a perfectly analogous case, and the specimen is still in my possession. Whenever the venous pulse is fully developed, it can not only be seen but also felt; and if the finger be placed on it we feel a INTRODUCTION.—PHYSICAL SYMPTOMS. 35 rhythmically repeated stroke. When the phenomenon is only slightly expressed, the pulsation can be seen, but can no longer be felt. Geigel has proved that increased pressure on the vena cava inferior is capable of making the cervical veins pulsate. The venous pulse may be a transitory phenomenon and disap- pear (especially towards the end of life), though all the condi- tions for its existence are still present, though even a simultane- ous insufficiency of the tricuspid and venous valves is present. This is rendered comprehensible by the fact that the quantity of blood and the rate of circulation both decrease with age, thus impairing the driving power immensely. Cases in which pulsa- tions have been felt to the right of the linea alba in the vena cava inferior are of the rarest occurrence, while a well-devel- oped case of cervical pulsation is almost always accompanied by a similar one in the liver, perceptible both by sight and touch. Bamberger's and Friedreich's sphygmographic investiga- tions were the first to establish the distinguishing characteristics of the venous and arterial pulse waves. Fig. 3. WmWM Pig. 4. ANAPICITROTOUS PtTl.SE IN THE INTERNA! T0GTJLAB VEIN (AFTER FBIKDBEICH). Close inspection of the sphygmographic curve shows that it is anadichrotous. The first and shorter rise in the ascending limb is the result of the contraction of the auricles, and is conse- quently presystolic; while the second, longer one, corresponds to the systole of the right ventricle. Friedreich has noticed dichrotism as well in the descending limb, and thinks that here 36 ROSENSTEIN.—DISEASES OF THE HEART. the slight rise at the end should be referred to waves reflected from the inner surface of the right ventricle itself. The pres- ence of a marked degree of anadichrotism or catadichrotism, or the presence simply of marked dichrotism depends upon the energy of the contractions of the auricle and right ventricle, on the one hand, and, on the other, upon the degree of tension in the walls of the veins, or, in other words, on the extent to which they yield. It should be here remarked, that the sphygmographic tra- cing taken from the pulsation of the liver does not always appear in the same form. Its ascending limb is indeed generally dichrotous, while we can only now and then perceive a slight dichrotism on the descending limb. A pulsation which is limited to the lowermost portion of the jugular vein, the so-called pulsation of the bulb, must, as regards its significance, be carefully distinguished from one which is visible more or less along the whole extent of the vein. This kind of pulsation occurs when the valves of the jugular vein, instead of occupying their usual position at the end of the vein, are inserted high up, and when at the same time there is insufficiency of the tricuspid valve. We cannot here attribute the pulsation to any failure of these valves to close properly, for they may even close with such distinctness as to produce a dis- tinct tone upon the ear of the listener—a tone to which Bamber- ger has given the name of " sound of the jugular valves." The last phenomenon we have to mention in regard to the cervical vessels, is one to which especial attention has been drawn by Friedreich—this is, that when the pericardium has been obliterated, a sudden collapse is perceptible in the hitherto full veins, occurring simultaneously with the diastole of the heart. When the adherent diaphragm rises with the shortening of the heart during systole, it draws the ribs and sternum inwards, but in the diastole these suddenly regain their position through their own elasticity, and thus at the same time as that in which this movement (which we can both see and feel) takes place, the veins instantly empty their contents. When, along with the adhesion of the pericardium, we find an extensive medias- tinitis, which drags upon or compresses the large venae innomi- INTRODUCTION.—PHYSICAL SYMPTOMS. 37 natae during inspiration, the usual conditions are reversed—the cervical veins, and especially the sinus venosus of the internal jugular, now exhibiting swelling, instead of during expira- tion. (Kussmaul.) Palpation in many ways controls ocular impressions, and is consequently used at the same time as inspection. It frequently happens that, by means of the touch, we can find the cardiac impulse in cases where inspection has failed to discover it. In the majority of emphysematous cases the covering of the lung renders the impulse imperceptible to the eye, while, by laying our fingers over it, we feel it at once. On the other hand, when an exudation of oily or elastic fluids in the pericar- dium is the object which prevents our seeing the movement of the heart, it is here equally imperceptible to the touch. Palpa- tion of the impulse of the heart makes us acquainted especially with its variations in intensity. There is indeed no universally applicable standard for this intensity, but with our fingers we can very well notice any abnormal resistance at the apex, such as that which accompanies hypertrophy of the left ventricle. For those cases, in which the strength of the impulse is so in- creased that the whole anterior thorax shakes with it, and the head of the auscultator is raised with every systole, and falls back with every diastole, here palpation is not necessary; but just in those cases of secondary hypertrophy of the left ventricle arising from abnormal resistance in the periphery (such as contraction of the kidneys or sclerosis of the aorta), where no special changes are discernible in the position or extent of the heart's impulse, increased resistance is of the greatest diagnostic value. At the same time we must not overlook the conditions which could entail an increased resistance, without any alteration in the heart itself, as for instance, better transmission of the stroke by solid. substances whether in the cavity or in the walls of the thorax. This indeed obtains for all pulsatory movements in the thorax, which palpation confirms as such, especially for the pulsa- tions of the aorta ascendens and pulmonalis already mentioned 38 ROSENSTEIN.—DISEASES OF THE HEART. in the paragraph on inspection. In the case of the pulmonalis especially, palpation supplements the inspection, since, besides the motion visible in synchronism with the systole, we can also feel the closure of the valves answering to diastole, whenever the necessary conditions are present for increased tension in the vessels. Quite as important as this increase of resistance, is to estab- lish, by palpation, a progressive decrease in the power of a once normal heart, from circumstances depending on changes in the substance, such as fatty degeneration, etc., or on a pericardial exudation. The investigator's finger can also discern abnormal vibrations which arise within or upon the heart. When, through hindrances to the stream, owing to changes in the lumen of the channels, whether in the outlets of the heart or in the vessels, eddying movements are produced in the blood, these may attain to such an intensity as to be not only heard, but even felt. This is especially palpable in stenosis of the ostium venosum sinis- trum as a whirring sound, which Laennec has termed " the cat's pur" {fremissement cataire); but it can occur in any valvular disease, and is, according to the disease, systolic or diastolic. But palpation can discern, not only those sounds which originate within the heart, but also those which are produced upon its outer surface. When the smooth pericardial surfaces become rough from the fibrinous deposit which takes place as a result of inflammation, and then rub against each other, a rubbing or grating sensation will be felt by the finger. Indeed, it is often an easy matter, by the sense of touch alone, to distinguish this friction sound from the so-called fremitus (fremissement). Both of these, however, are chiefly to be discerned when there is in- creased activity of the heart's action ; and at times they vary so greatly in intensity that they may even disappear for a brief time, although a moment before they were quite distinct. To distinguish a pericardial from a pleural friction sound, it is necessary to show distinctly the dependence, in the former case, of the sound on the movements of the heart. The means for distinguishing the two sounds will be more fitly described under the head of auscultation. This peculiar vibratory sensation (fremissement) can also be INTRODUCTION.—PHYSICAL SYMPTOMS. 39 felt on the larger vessels, especially on the right internal jugular. The impression is exactly similar to that which we receive from laying one of our fingers on a pianoforte wire, when a note has been struck, and is due to the vibrations of the walls of the vein, imparted to them from the vibrations of the blood. The con- sideration that the veins have a different-sized lumen along their course and at the termination in the sinus venosus, is quite sufficient to explain the existence of the eddies. Consequently we often feel the vibration even in perfectly healthy people. But slackness of the venous walls and a comparative emptiness of the vessel are the chief conditions which produce an increased intensity, this being the reason why it is chiefly to be heard in chlorotic and anaemic cases ; not that it is by any means con- fined to these diseases, or that it can be regarded as a symptom universally indicative of anaemia. The muscular contraction which takes place in the action of turning the head on its axis, narrows the lumen of the vein, and thus strengthens the sound. For the same reason, light pressure of the finger on the vein will also increase the sound, and even call it into existence, in cases where before it was not perceptible. However, the phenom- enon is not altogether confined to the veins of the neck, for we sometimes hear it or feel it in the peripheral veins. Of these, the femoral vein is the one in which the phenomenon is most often observed, not only in constitutional troubles which result in imperfect filling of the veins with blood, and a corresponding flaccid condition of their walls, but also in local conditions or disturbances which produce changes in the lumen of the vessel. The palpation of the arteries is of great importance in diagnos- ticating heart diseases ; on the one hand, from the judgment we can form thereby, as to the condition of the walls of the vessels ; and on the other hand, more important, from the changes which the pulse undergoes as a result of alterations which have taken place in the circulation. The immediate result of diseases of the arterial walls is decrease of elasticity, especially when in- flammatory processes have acted on their tissue. This loss of elasticity impairs the resistance the artery can offer to the forward-pressing wave of blood, and thus the vessel undergoes a lasting tension which ultimately dilates it. But as the arteries 40 ROSENSTEIN.—DISEASES OF THE HEART. are fixed in the direction of their length, the dilatation must result in windings and twistings, and if this assumes large pro- portions, we can even see it on the relatively superficial vessels, while the slightest trace of it is always palpable. In itself this tortuousness of the arteries signifies nothing more than a loss of vascular elasticity, and can occur to almost any extent, under the name of aneurysma cirsoides, unaccompanied by any athe- roma. Endoarteritis, however, is the commonest cause of this loss of elasticity. The inflammation acts chiefly on the intima coat, but is still accompanied by considerable thickenings in the adventitia. The resistance of the vessels is thereby increased, and consequently we feel a peculiar hardness of the wall in addition to its tortuousness. It is highly important to be aware of this condition of the vascular walls, because it creates hinder- ances in the circulation, the mechanical effects of which must eventually reach the heart; and because, further, similar changes may at the same time attack the aortic valves. By means of Marey's sphygmograph we are enabled to observe these altera- tions in elasticity, and record them graphically ; and Landois has ascertained, by experimental research, the changes which take place in the tracing of the pulse in atheroma. The normal pulse is catadichrotous, i.e., the tracing exhibits a moderately sharp ascent, corresponding to the dilatation of the vessel, and a descent, corresponding to its contraction. The latter is varied by two or more minor ascents, caused partly by the recoil wave, which is excited, as Landois has shown, in the vessels during the systole, and begins with the aortic valves, and partly by the vibrations of the elastic walls. The notches in the curve due to elastic vibrations are altered (i.e., either diminished or obliterated) in diseases which affect the vascular elasticity; and the eleva- tions corresponding to the recoil are also affected, since they, too, are partly under the influence of this elasticity. After some time, general extension of the process produces secondary changes in the heart, through which, in the same space, a larger quantity of blood flows into the aorta with every systole. This and the diminution in height of the elevations arising from loss of elasticity, produce a curve for atheroma which differs from the normal curve principally in the circumstance that a plateau- INTRODUCTION.—PHYSICAL SYMPTOMS. 41 like elevation shows itself on the ascending limb—the curve, in other words, is anachrotic—while on the descending limb there is only a very small elevation, produced by the recoil. Fig. 5. In the vascular changes, just described, we have found that tortuousness and hardness were easiest distinguished by palpa- tion, whereas the graphic method brought the variations of the pulse most clearly before our eyes. But diseases of the valves and cardiac muscle also produce changes in the character of the pulse, which are directly perceptible to the touch ; these are chiefly such as concern its duration, frequency, and tension. It is perfectly plain that similar and as marked variations in the pulse can also be produced by other diseases besides heart and pericardial diseases. A description of all the causes which pro- duce the various divergences would require a separate treatise on the pulse, and is here quite out of place. We shall accord- ingly confine ourselves to those forms which occur as symptoms of heart disease. Alterations of rhythm occur as inequality, when waves of even dimensions do not follow one another—as irregularity, when the waves do not follow at regular intervals. Fig. 6. Unequal pulse. Unequal and irregular pulse. The irregular pulse may be subdivided, according as entire contractions of the heart are completely wanting and no eleva- 42 ROSENSTEIN.—DISEASES OF THE HEART. tion of the artery at all can be felt (pulsus deficiens), or as some beats of the heart are too weak to make the wave palpable at the periphery where we usually feel for it (p. intermittens). Some- times it feels as if, between two equal and regularly following elevations, a dissimilar one were inserted (p. intercurrens or inci- dens); sometimes two or more beats of the heart are combined in forming a double or trebly compound pulse (p. coturnisans). Amongst the last-mentioned variations from the normal rhythm especial interest attaches to that form which Traube has de- scribed under the name of pulsus bigeminus. This consists of two short beats, followed by a long pause, and each of the two beats corresponding to a contraction of the heart, in contradis- tinction to a dichrotous pulse, in which the double beat belongs to a single contraction of the heart. Traube's conclusion, based on his experimental investigations, is that this form occurs when the heart is freed from the influence of the spinal division of its inhibitory nervous system, while the cardiac division, still intact, is irritated to a greater degree than usual.1 This pulse may consequently be regarded as a very unfavorable prog- nostic symptom. The pulsus alternans (a secondary form of the bigeminus, and also described by Traube) differs from the ordinary rhythm in as far as a low pulsation follows on every high one, and a pause after the low pulsation is longer than that preceding it.2 The following case, which came under my treatment, seems worth communi- cating. The rhythm was very similar to that of Traube's pulsus bigeminus, but still it is not perfectly analogous. Otherwise, however, as may be seen from com- paring the cardiac impulse, it was a phenomenon dependent on the heart's action, and cannot be referred to mere changes in the vascular walls. This is not affected by the fact that the tracing was only taken on one side—namely, from the radial artery of the paralyzed arm. The case itself was as follows: Welling, aged 28, a painter, was dismissed nine years previously from military 1 Ph. Knoll disputes this explanation of the pulsus bigeminus, because he saw it continuing after he had injected a large dose of atropine. He seeks to explain it by the premature occurrence of another systole, before the heart, which has emptied its con- tents in the preceding vigorous systole, has time to take in its normal quantum of blood in diastole. 2 Comp. Berliner klinische Wochenschrift, 1872, No. 16. INTRODUCTION.—PHYSICAL SYMPTOMS. 43 service, on account of " palpitations of the heart," as he alleges. During these nine years he was generally able to work, till one day, three months before being received into hospital, he fell down suddenly, losing consciousness, but without any symptoms of paralysis. After three weeks' confinement to bed he went to work again. Yesterday, October 30th, felt ill while standing on a scaffold, came down to the ground, but then fell, and was paralyzed on one side. He was received into hospital in the following condition: Powerfully built, large bones, and well- developed muscles. Mucous membranes rather pale. Patient is confused, but not perfectly unconscious. When loudly addressed he answers, incomprehensibly in- deed, but still showing that he has heard the question. Right angle of the mouth lower than left, puts out his tongue straight, soft palate normal, motion of the eyes intact, pupils evenly dilated. The left arm is completely and the right partially paralyzed. Sensibility likewise diminished on the right side. Thorax normally curved, the type of respiration abdomino-costal; twenty respirations to the minute. Rhythm regular. Cardiac impulse strong—can be seen and felt be- tween sixth and seventh ribs, within and without the mammillary lines of both sides. Rhythm of cardiac impulse is abnormal—on one impulse follows a second weaker one, divided by a longer pause from the next beat than from the previous one. The dulness begins on the lower border of the third rib, is 9 cm. high, 14 broad, extending externally to the left mammillary line. With the stethoscope over the apex of the heart, a loud systolic and weaker presystolic blowing sound is audible. Over the ostia of the larger vessels the second sound is double. The left radial artery of medium calibre, slightly tortuous; the pulse full, and 56 beats to the minute. The annexed curve gives the rhythm. Fig. 8. IM1MMIIMII (No tracing could be taken of the pulse on the unparalyzed arm, on account of incessant convulsive movements.) In regard to other organs, the lungs were normal, the liver enlarged. Urine contains a great deal of albumen. Next day the pulse grew more rapid, the respirations intermittent, and the rhythm of the pulse less distinct, the paralytic symptoms unchanged. On the third day patient died. Of the results of the autopsy I shall only mention those relating to the brain and heart: Calvarium normal, vessels of the dura mater injected; after removal of dura superficial extravasations of blood are visible, about a centimetre in breadth. Pia mater easily removable. Gyri flat, and sulci badly expressed. On the right side the substance of the brain at a depth of one centimetre is infiltrated with blood, and as we go deeper the extravasation becomes more plentiful. The right lateral ventricle is completely filled with a coagulum. Corpus striatum and thalamus opticus on this 44 ROSENSTEIN.—DISEASES OF THE HEART. side are converted into a pulp of blood. The left side is free from extravasation. The arteries of the Sylvian fissure show nothing abnormal. The heart is 11 cm. long, 12 broad, and 27 in circumference. The free border of the mitral valve is thickened, wrinkled, and beset with a fringe of long excres- cences. The opening allows three fingers to pass through easily. The points of the papillary muscles are converted into connective tissue. The borders of the aortic valves are slightly thickened, and along the line of closure beset with small excres- cences. Other valves are normal. Changes of the normal rhythm, too, are generally connected with anomalous frequency of the cardiac pulsations. Both the slow pulse (p. rarus), and the hurried (p. frequens), and at the same time irregular, are most commonly observed in diseases of the cardiac substance and of the vessels which supply it (the coronary arteries), and more rarely in valvular diseases and general atheroma. But these irregularities also occur independ- ently of any perceptible pathological anatomical changes in the heart, expressing pure neurosis, as in violent reflex excite- ment of the vaso-motor centre. Thus, in a case of intercostal neuralgia, I have observed a long duration of an unequal and irregular pulse, which, when accompanied by an accidental murmur, aroused suspicion of valvular disease. Whether their occurrence in infectious diseases, especially typhoid fever, is un- connected with the coarser changes of the cardiac substance, remains doubtful. Changes of frequency without similar one3 of rhythm are brought about by more general influences—age, posture (horizontal or standing), time of day, excitement, fever, etc. The changes in celerity affect the relations of duration in which the diastole and systole stand to one another. The abnor- mality consists in the shortening of the time during which the vessel remains dilated by the wave of blood driven into it with the cardiac systole; the explanation is, that the maximum of dilatation is quickly reached and equally quickly foil owed by the contraction of the vessel. Vierordt, and, still more accu- rately, Landois, have expressed the normal relations in celerity for the different arteries in actual numbers ; no estimates, how- ever, have yet been made of these relations in disease. Insuffi- ciency of the aortic valves is the disease, par excellence, which INTRODUCTION.—PHYSICAL SYMPTOMS. 45 unites all the conditions favorable to the production of this form of pulse. The physical causes are, on the one hand, the enor- mous quantity of blood which the hypertrophied and abun- dantly-filled left ventricle drives into the vessels with each sys- tole, and, on the other hand, the easy regurgitation allowed by insufficient valves. The reversed physical conditions prevail in stenosis of the ostium aortse ; in this condition, in which a smaller quantity of blood is driven with each systole into a tense system of vessels, the pulsus tardus is encountered. By the force we have to counteract in trying to compress the artery, we can measure the changes in its resistance, or in the tension of the pulse, and thus distinguish between a hard and a soft pulse. These changes relate to the tension of the artery during its diastole and systole. The tension is directly depend- ent, as a rule, on the amount of blood in the vessels, and yet it does not always bear a fixed relation to it. The same affections of the venous and of the arterial cardiac ostia produce exactly opposite effects upon this tension. Thus, for example, stenosis of the left ostium venosum renders the pulse small and soft, while stenosis of the aortic ostium renders it small and hard. Kussmaul has described, under Griesinger's name of "para- doxical" pulse, a peculiar form which has been repeat- edly observed in cases of excrescent mediastino-pericarditis. For inflammation sometimes attacks not only the serous, but also the fibrous stratum of the pericardium, and produces fibrous formations projecting into the mediastinal connective tissue, and thus throwing tendinous strings from the reflection of the peri- cardium to the large vessels, such as the aortic arch and the venae innominataB. In such cases it often happens that the trac- tion which the sternum exerts on these cords during inspiration produces a displacement and stretching of the vessels, sometimes even a compression ; this renders the pulse very small and some- times even stops a beat. The peculiarity of this clinical phe- nomenon is that, without any appearance of disturbance in the cardiac action, we have an apparently irregular pulse, which becomes smaller, or disappears during inspiration. The irregu- larity is, however, merely apparent, for the pulse acts in the same way during every inspiration. 46 ROSENSTEIN.—DISEASES OF THE HEART. Though the explanation of this clinical symptom by the par- ticipation of the mediastinum in the pericarditis is well founded, still we must not ignore the fact that this pulse can be produced by other diseases besides this one. Apart, too, from the influ- ence of increased negative pressure on the left ventricle, arising from stenosis of the respiratory tract, and displaying itself, accord- ing to its intensity, by diminution or interruption of the pulse during inspiration, the pulsus paradoxus can be produced by chronic pericarditis alone, without any complication of the medi- astinum ; cases of this kind have been observed by both Traube and Baeumler. For these cases, also, Baeumler endeavors to find an explanation in the alteration in intrathoracic pressure and in the resulting variations in the amount of blood which the vessels contain. Percussion enables us to detect the abnormal symptoms pro- duced by alterations in the volume or position of the heart. Owing to the great freedom of lateral motion allowed to this organ, even under normal conditions, alterations take place in its position, when one turns over on his side, after lying on his back. So the first necessary condition for forming a correct esti- mate of the results of percussion, whether disease be present or not, is to put the patient in the recumbent position (lying on his back) during examination. A second and equally important precaution, in making a diagnosis of the changes in the area of superficial dulness, is to test the movableness of the anterior borders of the lungs. When one or both of these borders is adherent, where the lung is contracted, or where that part which lies next the pericardium is infiltrated, then we may find the area of superficial dulness (according to the point at which the adherence has taken place) greater or smaller than normal, but still unaccompanied by any change in the size of the heart. The height of the dia- phragm, too, must always be estimated and taken into account; for the extent of the anterior surface of the heart coming into contact with the chest is increased or diminished according as the diaphragm stands higher or lower, and thus variations in the INTRODUCTION.—PHYSICAL SYMPTOMS. 47 size of the area of absolute dulness are produced, which are not at all the result of variations of the heart's volume. Although this apparent atrophy and hypertrophy of the heart, produced by the causes mentioned above, may be disregarded and excluded from the diagnosis, the symptoms of actual enlargement, on the other hand, vary in their significance according to the region in which they preponderate. When the left side of the heart is enlarged, both the superficial and deep-seated dulnesses are intensified below and to the left; the same takes place over the sternum and beyond its right border when the right side of the heart is enlarged. It must not be forgotten that the absence of all percussional symptoms does not at all exclude the possibility of hypertrophy. Even very considerable hypertrophy (especially of the right side of the heart) can escape detection by percussion, if the lungs are emphysematous ; and that, too, when along with palpation we percuss heavily, and proportionately to the resist- ance. And besides, where the right heart is enlarged, the limits of dulness on percussion may be somewhat extended toward the left, owing to the more horizontal position which the organ then assumes; this is observed, for instance, in stenosis of the left ostium venosum. The shape of the normal area of dulness becomes somewhat modified when there is fluid in the pericardial sac. The shape assumed will then be a triangle, with its obtuse apex pointing upwards, and its base below; for the heart, on account of its higher specific gravity, occupies the lower space, and the collec- tion of fluid takes place at first in the upper part, corresponding to the junction of the pericardium and the large vessels. If the exudation is large, provided there was no pre-existing adhesion of the edges of the lungs, the apex of this triangle may reach up to the first intercostal space ; usually it does not reach beyond the second space. The right side extends downwards from the third rib and out beyond the right sternal border, and may even go as far as the right nipple ; the left side stretches down over the left nipple till it reaches the axillary line. Height and breadth of both regions of dulness are altered, as well as their figure. Gerhardt has called attention to the influence exerted by change of posture in these relations as well as in the others. He 48 ROSENSTEIN.—DISEASES OF THE HEART. has shown that in the standing posture the region of superficial dulness is more extensive than in the recumbent posture. Small quantities of fluid, so much even as 3 or 4 oz., may be present in the pericardium, though we are unable to detect it by per- cussion. Diminution in the area of superficial cardiac dulness is, in the majority of the cases where it occurs, merely apparent, and is produced by interference of the lungs, especially in connec- tion with a sunken diaphragm. When the stomach is greatly distended, the transmission of its tympanitic sound induces an upward displacement of the limits of the deep-seated dul- ness, and thus makes it appear as though these were reduced. When the pericardium contains gas (pneumopericardium), the superficial dulness entirely disappears, and is replaced by a sound, which is generally metallic in character. Since fluid very soon follows the gas, a line may be found with a sharp me- tallic sound on one side, and a dull sound on the other; the position of this line will naturally shift as the patient changes his posture. When auscultating the heart in disease, we shall meet with many alterations in those sounds which we have already studied in their normal condition. The alterations affect either the purity of the sounds, their clearness, the limits of their extent, their intensity, or their timbre; but the most important point is, that we shall find the sounds accompanied or replaced by murmurs. The definition of the sounds depends chiefly on the uninjured vibratory powers of the valves. Even trifling structural changes in these, which have no material influence on their function, can make one or the other cardiac sound appear less distinct and defined to the ear, and hence give it the name of indefinite. The changes in clearness are quite different, and have, like those of intensity, a complicated origin. Besides vibratory power, the valves must also have a certain tension, and the parts which lie over the heart must be good conductors of sound. Any varia- INTRODrCTION.—PHYSICAL SYMPTOMS. 49 tion of a single one of these conditions will render the cardiac sounds clear or dull, plainly or feebly audible. As a general rule, a clear sound is plainly heard, and a dull sound feebly; but still a dull sound may be plainly heard, since bad conduction will dull even an intense sound, and, on the contrary, an origin- ally weak sound can be rendered distinctly audible by improved conduction. All sounds of the heart are rendered abnormally loud, or strengthened, when the work of the whole heart is in- creased, as, for instance, after physical exertion. The first sound is heard particularly loud at the apex, when the difference of tension in the auriculo-ventricular valves, between the end of the diastole and the beginning of the systole, is very great; this is most marked in stenosis of the left ostium venosum. In cases of very marked hypertrophy of the left ventricle, the first sound is very loud over the apex, accompanied by a metallic click (cliquetis metallique). The muscle sound probably contributes in a meas- ure to this increased loudness. We hear the second sound very often much louder than usual over the ostia of the large vessels. Provided we exclude the possibility of an improved conducting medium, such as infiltrated pulmonary tissue, or a vessel brought into close contact with the chest, by contraction of the lung over- lying it, this loud second sound must be construed as a symptom of greater tension in that vessel, over the ostium of which it is heard. The second sound over the aortic ostium is, as a rule, relatively louder than that over the pulmonary artery. Hence the increased intensity of the second sound of the pulmonalis implies an increased tension in the pulmonary artery, due to the exist- ence of an obstruction in the lesser circulation. Increase of the intensity of the second aortic sound points to abnormally high tension in the aorta, as results from increase of power in the left ventricle, provided, of course, that the semi- lunar valves are still capable of performing their functions. When the sounds display an increase in intensity, they are also audible over a greater area. To hear the normal cardiac sounds on the back (especially in the left interscapular space) is only possible in the case of slenderly-built children and women, while the sounds of a generally hypertrophied heart are audible on the back in every case. The fact that we can hear the cardiac VOL. VI.—4 50 ROSENSTEIN.—DISEASES OF THE HEART. sounds over a large surface in phthisical cases depends entirely on the presence of infiltrated pulmonary tissue as a better con- ducting medium. All sounds of the heart are abnormally weak, when this or- gan contracts but weakly, as in the case of disease of its sub- stance due to inflammation or fatty degeneration. The sounds are especially dull when the conduction of the sounds is dead- ened—by extensive emphysema of the overlying parts of the lungs, by intervention of fluid between the pericardium and heart, by cedematous infiltration of the external supracardial soft parts, or, finally, by a large panniculus adiposus. Abnormal weakness of the first sound over the apex occurs either when the tension of the auriculo-ventricular valves is very small, which may be caused by general disturbances, such as typhus or typhoid fever, since these produce changes in the contraction of the papillary muscles, or it may occur when the difference between the final diastolic tension of these valves and their commencing systolic tension is extremely small, as happens when the aortic valves are defective. In this case, the first sound over the apex can disappear completely. Abnormal weakness of the first sound on the large vessels occurs when their tension is diminished; in the case of the aorta, for instance, it occurs when the mitral valve is defective, and does not allow so much blood to be propelled into the vessel by the contracting ventricle. The second sound is either heard feebly or not at all over the large vessels, when there is stenosis of their ostia. A change in the timbre of the heart sounds, especially one to a metallic timbre, will be observed when at the same time a large space filled with air, and provided with smooth walls, happens to be in the immediate neighborhood of the heart; such a space may be found in the pericardium itself (pneumo-pericardium), or at times in the left pleural cavity (pneumo-thorax), or, most rarely of all, in a pretty large cavity, occupying the substance of the lung, and lying in close proximity to the heart. In pneumo- pericardium, fluid usually soon makes its appearance in the per- icardial sac in addition to the air, and so gives rise to splash- ing sounds of a metallic character, resembling the sounds INTRODUCTION.—PHYSICAL SYMPTOMS. 51 produced by water when it is allowed to fall in drops from a certain height into a hollow vessel. I once heard these sounds with peculiar distinctness in a case of pneumo-pericardium, due to the existence of a communication between the pericardial sac and the stomach, through the diaphragm (from ulcer of the stomach). Reduplication or division, as the case may be, is a peculiar anomaly of the cardiac sounds, which is observable under both normal and pathological conditions, and may affect both sounds ; it is characterized by the existence of a rhythm, which was known even to Bouillaud, and by him described under the name of bruit de rappel, on account of its resemblance to the military signal of that name. We speak of reduplication of the sound when additional short pauses intervene between the separate sound-elements ; on the contrary, we mean by division the transition of one sound into the other without any interval at all. Potain was the first (see bibliographical list) who called attention to the physiological frequency of the phenomenon. He showed that these functional physiological reduplications and divisions are dependent upon the influence which the different phases of respiration exert upon the relations of the intrathoracic pressure, and consequently upon the circulation. Thus, for example, this influence shows itself in the fact that expiration retards the flow of blood in the veins, while inspiration enfeebles the action of the left ventricle, and so diminishes the pressure in the aortic system. If either force preponderates, both auriculo-ventricular valves, or both semi-lunar valves, instead of closing synchronously, will close one after the other, thus giving rise to a reduplicated sound. This accords with the fact that it is possible, by artificially hinder- ing or facilitating the breathing, to alter the relations (as regards time) which the reduplication of the sounds bears to the respira- tory phase. The phenomenon, when the symptom of disease, can originate in asynchronism of the closure of the separate valves, perhaps even of the points of the valves, and especially in a more jerky and less energetic contraction of the papillary muscles, arising from nervous disturbances. The quick, transitory man- ner in which the symptom often occurs, and its disappearance as 52 ROSENSTEIN.—DISEASES OF THE HEART. soon as the heart's action revives, speak in favor of this explana- tion. But differences of tension, totally independent of nervous and respiratory influences, can take place in the aorta and pul- monalis, especially in connection with the second cardiac sound, producing asynchronism of the closure of the valves, and thereby a division of the second sound. To Geigel is due the credit of having suggested that the division of the second sound is induced by the inequality of tension in the aorta and pulmonary artery, caused by the unequal quantities of blood they contain. This is often heard in stenosis of the left ostium sinistrum, though (as Guttmann properly observes) not nearly as often as Geigel as- serts. In fact, in the last cases, if the patient exert himself somewhat, we hear a diastolic murmur instead of the divided sound. Wherever the transition from a doubled or divided sound to a murmur is very slight, the pathological significance of the symptom is undoubtedly that of a murmur. This is, in all probability, too, the case, when the interval between the two parts of the double sound is particularly long. The rarest cause which has been adduced for these doubled sounds is an actual asynchronism of the contraction of the two ventricles. This does not appear at all probable from the ana- tomical arrangements of the muscles ; but still it is possible, and has been witnessed by observers, such as Leyden. In this case we have a doubled cardiac impulse as well. That form of reduplication of the second sound, in which the second of the couplet follows immediately on the second ventri- cular sound, is entirely different both in its mode of origin and in its diagnostic value. It is caused by the diastolic recoil of the chest after it has been drawn in by the systole ; this latter pro- cess, as Friedreich first pointed out, is a symptom of chronic obliterating pericarditis. All cardiac murmurs must be divided into two classes, namely, those that have their origin inside the heart (endo- cardial), and those which arise on its external surface (exo- cardial). The endocardial are subdivided into organic, or those which are connected with a palpable change in the valvular apparatus, or in the cardiac substance ; said.functional, or those which take place independently of any perceptible change in INTRODUCTION.—PHYSICAL SYMPTOMS. 53 these tissues. The mode of origin is probably the same for all murmurs; they originate by oscillations in the blood itself (the so-called "eddies"). It is doubtful whether unequal vibrations of the valves can also produce murmurs. The old theory, that murmurs are produced on the rough surfaces of the valves and vessels by friction with the blood, is physically untenable since the investigations of F. Neumann, Poiseuille and others on the motion of fluids in closed vessels have proved that the extreme peripheral layer of the fluid merely moistens the walls, and must consequently be at rest. This view, too, is in perfect accordance with a series of well-known pathological facts; as, for instance, that no murmur is to be heard in extensive atheroma of the vascular walls (provided the atheroma is not complicated with alterations in the lumen of the vessels), and further that the maximum intensity of a murmur is not to be heard where we should have to suppose the greatest friction. Thus this fric- tional origin of the murmurs must be regarded as wholly dis- proved—while, on the other hand, the oscillations, which take place in the blood, during a transition of the stream through openings of an unequal lumen, produce a friction between the particles of the fluid itself. In the transition from a narrow part a murmur originates immediately in the succeeding part. After Corrigan had referred the origin of the proper cardiac murmurs to movements in the blood, and had initiated an experiment which was to have proved this, Kiwisch, Heynsius, Weber, and later Chauveau, Marey, Thamm and Nollet furnished the experi- mental proof necessary to establish the oscillation theory on a firm basis. Especially the investigations of Heynsius and Nollet, in opposition to the opinions of Weber, Chauveau and others, have proved with certainty that the primary vibrations which take place in the blood itself (the so-called tourbillons, which originate during the transition of the stream from a narrower into a broader part of the vessel) are the real causes of the mur- murs, and that the influence of tension and lateral pressure on these motions was nothing, while the influence of the rapidity of the stream was very great. The fact, which Weber discovered, and Nollet and Tliamm confirmed, that, if the stream be only rapid enough, murmurs may be produced even in a glass tube of 54 ROSENSTEIN.—DISEASES OF THE HEART. uniform diameter, quite disproves Chauveau's theory that the origin of the murmur lay in a veine jiuide with its molecular oscillations, or, as Paul Niemeyer expresses it, in the compression of a stream through a narrow opening ('' Press-strahl''). Clinical experience, too, harmonizes with the physical basis, and lays especial weight upon the rapidity of the stream. All murmurs which arise in the heart are intensified by exertion, and weak- ened when the heart's power decreases. In cases of stenosis of the left ostium venosum, we can sometimes only succeed in hearing the murmur after making the patient exert himself vig- orously, and even the loudest murmurs become inaudible towards the end of life, when the activity of the heart has begun to fail. It is possible that the undoubted influence, which change of posture may produce in the audibleness of the endocardial mur- murs, may be connected with changes in the rapidity of the stream. It is with perfect correctness that Sidney Ringer and others have observed that, in some cases, when the patient is in the horizontal posture, a loud murmur is audible, which completely vanishes, or becomes very indistinct, when the vertical posture is assumed. In general, however, it appears to me that the sitting posture is most favorable for hearing these endocardial murmurs. But in dubious cases it is better to let the patient exert himself a little, and then examine him in different postures, before giving one's final opinion on the presence or absence of a murmur. After the presence of the murmur has been fully established, we must next determine, in order to give it its proper clinical significance, whether it is exo- or endocardial. The following symptoms will serve as data for making this distinction: all endocardial murmurs are exactly simultaneous with one or other of the cardiac sounds, being either systolic, diastolic, or both; the exocardial, on the other hand, are heard after or between both sounds, and hang behind ; the endocardial are of a various char- acter, blowing, breathing, scratching, or rasping; the exocar- dial are always rasping, however much the intensity may vary. Exocardial murmurs are generally heard at first over the base of the heart, afterwards at the apex and over its whole extent; endo- cardial do not increase so much in extent, being more local and INTRODUCTION.—PHYSICAL SYMPTOMS. 55 fixed; exocardial, further, if at all intense, can always be felt, which is not the case to such a degree with endocardial murmurs. Exocardial murmurs may also be heard synchronously with the movements of the heart, without there being any affection of the pericardium. Those murmurs which are produced by the rub- bing of pleural surfaces upon one another in the vicinity of the heart, generally vary in intensity with the movements of respira- tion (Skoda). When it has been decided that the murmur belongs to the endocardial class, the next thing is to learn whether its origin is organic, i. e., the result of anatomical changes, which have pro- duced disturbances in the cardiac functions, or functional and ac- cidental, i. e., independent of coarse, anatomically perceptible changes. The functional murmurs are almost always of the same blowing and sighing character : they occur most frequently over the left ventricle, and are heard as often over the base as over the apex of the heart, but in many cases their greatest intensity is exactly over the ostium of the pulmonary artery. Almost all coincide with the systole, and are dependent upon it. The most important difference, and the one which alone affords perfectly reliable evidence, is, that the organic murmurs are almost always accompanied by corresponding symptoms of cardiac disturbance, that they in fact bring with them regularly more or less extensive alterations in the size of the heart, while no such change is per- ceptible in connection with functional murmurs. In the mean- while we must not forget, that on the one hand changes of vol- ume which are actually present, dilatation of the right auricle for instance, can escape detection by percussion, owing to complica- tions such as emphysema of the lung; and that, on the other hand, temporary changes of volume, which afterwards disappear—for example, the dilatation we have in strongly developed chlorosis— can occur without any coarse anatomical changes of the vascular apparatus. This shows that it is not sufficient to take cognizance merely of the secondary changes of volume, but that on the con- trary we should direct special attention to the intensity of the second vascular sound (in the aorta and pulmonary artery). It should also not be forgotten that, at the apex of the heart, mur- murs of an endocardial character may be heard, the origin of 56 ROSENSTEIN.—DISEASES OF THE HEART. which is to be referred to the lungs (Wintrich's aspiration mur- murs). When all doubts of the organic nature of the murmur have been set aside, the next step, in order to ascertain its more precise signification, is to determine exactly the cardiac phase with which it is synchronous. A skilful practitioner will be at once able to de- cide, from the rhythm, whether the murmur is systolic or diastolic. The safest method, however, for deciding this is, while auscul- tating, to lay the finger on the impulse of the heart, or, if this be not palpable, on the carotid artery ; it is clear that the radial artery would not serve this purpose, as it does not beat synchronously with, but a little later than, the cardiac impulse. But we meet with organic murmurs which are audible not during the systole alone nor during the diastole alone. The fact is, all organic murmurs last longer than normal sounds, and although many murmurs, not- withstanding their longer duration, allow us to distinguish both the short interval between the first and second sounds, and the longer interval between the second and following first sound, still we find others which are not sharply confined to one or other of the car- diac phases, but extend into the succeeding interval; for example, a murmur can be protracted from the diastole to the next systole, so that the first cardiac sound comes in immediate connection with the murmur. This very so-called presystolic murmur has great importance attached to it, since it is a specific symptom for sten- osis of the left ostium venosum. It is a matter of choice, if any one likes to imitate Gendrin, and distinguish a peridiastolic as well as a presystolic murmur, and a perisystolic one, when a short murmur extends into the interval between the first and second sounds ; but these distinctions have no claims to practical worth. Many physicians lay great weight on ascertaining whether a cardiac sound is to be heard as well as the murmur, since in special cases we can from this draw conclusions as to the degree in which the valves are affected. We have already men- tioned Gendrin's method of raising the ear slightly from the disc of the stethoscope during auscultation, and thus rendering the sound more and the murmur less audible, and we can recommend it for doubtful cases of this kind. However, the distinction is seldom of any practical importance ; for, as Friedreich has shown, INTRODUCTION.—PHYSICAL SYMPTOMS. 57 in most affections of the mitral valve, even when the degenera- tion is far advanced, we can hear a cardiac sound along with the murmur. (When the aortic valves are insufficient, the inten- sity of the second sound in the carotids is the simplest and safest aid in diagnosis.) After we have determined the cardiac phase with which the murmur is synchronous, to localize it still closer we must look for the position of the maximum intensity. From what we have already said of the positions, which were most suitable for auscultating the places where the different sounds originate, it is evident, that, if we hear a murmur in its maximum intensity over one of these positions, the murmur originates here as well. For instance, a murmur with its maximum intensity at the apex is referred to the mitral valve ; but if it is most audible on the fifth right sterno-costal symphysis, we refer it to the tricuspid ; when at the border of the sternum in the second right intercostal space, it is assigned to the aortic valves ; and to the valves of the pul- monary artery, when in the same space on the left side. For the interpretation of the different murmurs we may lay down the general rule, that murmurs which are heard loudest over the position for auscultating the auriculo-ventricular valves, are to be referred to insufficiency of these valves, if systolic, but to stenosis of the same if diastolic or presystolic; when the great- est intensity of a murmur is over an arterial ostium, it is referred, if systolic, to the semi-lunar valves of this ostium, but if it is dias- tolic in the same place, or in the direction in which the stream of blood flows, it denotes insufficiency of the semi-lunar valves. I have purposely added the words "in the direction in which the stream of blood flows," since murmurs produced by insufficiency of the semi-lunar valves are in most cases heard more distinctly over the sternum than over the arterial ostia. In fact, we should not be content with merely establishing the point of greatest inten- sity, but we should take into account as well the direction in which the murmur is propagated. Now, all murmurs which arise in the heart are propagated in the direction in which the stream of blood flows. The murmurs of regurgitation arising from insufficiency of the mitral are propagated in the direction of the left auricle and auricular appendix. For this reason the 58 ROSENSTEIN.—DISEASES OF THE HEART. systolic murmur, in connection with insufficiency of the mitral valve, is often as audible, or even more audible at the level of the pulmonary ostium (on the anterior wall of which the left auricular appendix lies) than at the apex of the heart. The mur- murs, on the contrary, which are heard from stenosis of the left venous ostium, follow in the direction of the stream towards the ventricle, and reach their maximum intensity at the apex, some- times even to the left of and externally to this. As the mur- murs may easily be transmitted from one arterial ostium to the other, special attention should be given to their propagation along the courses of the aorta and pulmonary artery. We have already stated that murmurs are chiefly influenced by the rapid- ity of the stream, and are quite independent of anatomical causes. Hence, it is quite clear that from the intensity we can draw, in general, no conclusions as to the degree of the valvular changes which have led to it. Auscultatory phenomena, closely related to cardiac diseases, are also to be found on the vessels of the neck and extremities. Under normal conditions two sounds only can be heard in the large vessels near the heart, in the carotids and the subclavian artery, but not in the more remote vessels. The first of these sounds arises from the vibrations of the vascular walls, produced by the alteration of tension between systole and diastole ; the second, on the contrary, is transmitted from the semilunar valves. Thus the greater this difference of tension is, the louder we hear the first sound, and that not only on the vessels near the heart, but also on the more peripheral ones. Insufficience of the aortic valves is the disease which gives rise to the greatest difference of tension between systole and diastole, and in such cases the first sound can be heard on the volar arch and dorsal artery of the foot, and other small peripheral arteries, while normally it can only be heard in the abdominal aorta, but not in the crural artery. Cervical murmurs may arise in veins as well as in arteries, or they may be only transmitted. When the aortic valves are affected it is easy to regard a murmur heard in the carotids as transmitted, and thus systolic if the aortic affection be stenosis, and diastolic if insufficience. Often we perceive a diastolic mur- mur over the aortic ostium, but are unable to detect it on the INTRODUCTION.—PHYSICAL SYMPTOMS. 59 carotids, where we hear in its place the second sound. In such cases there is only partial degeneration of the valves, and the murmur we hear over the ostium conceals the sound, which is in reality still produced; hence the cause of the murmur lies in some changes which do not result in total incapability of closure in the valves. The systolic murmur heard in the caro- tids during aortic insufficience may be produced in the cervical vessels also by irregular vibrations; for the walls lose in elas- ticity from the continuous high tension to which they are exposed. The arterial murmurs are intermittent, or at least louder dur- ing the corresponding cardiac phase, and thus differ from the continuous venous murmurs, which are to a great extent inde- pendent of the cardiac movements; but, on the other hand, these latter are intensified by respiration, and especially by inspi- ration, which increases the rapidity of the circulation in the veins, and thus hastens their exhaustion. But even venous mur- murs may be somewhat intermittent in character. Chauveau was the first to show that they are either audible only during the diastole, or, if continuous in character, they can be more dis- tinctly heard during the diastole. He attributed this rhythm to the fact that during the diastole there was a diminution in the pressure of the blood within the vein, and therefore an increased rapidity of current. By unskilful auscultation, or by purposely pressing the stethoscope on the arteries, we can produce artificial murmurs ; and, as we have already remarked, in the same man- ner, the slight pressure the omohyoid muscle and its fasciae exert on the underlying jugular vein in turning the head, suffices to pro- duce murmurs in this vein, which greater compression will cause to disappear. These murmurs are produced by exactly the same factors which we have mentioned in our analysis of the palpable vibration of the veins ; and so it is easy to understand that they are not necessarily connected with local heart disease ; but that they are rather related to certain general conditions which directly influence the quantity of blood in the veins, their tension, and the rapidity of the current. That venous murmur, however, which is caused by tricuspid insufficiency, and which is there- fore in immediate connection with a cardiac phase (the systole), 60 ROSENSTEIN.—DISEASES OF THE HEART. bears a direct relation to diseases of the heart. Where there is insufficiency of the valves of the veins, without coincident tri- cuspid insufficiency, this venous murmur can be both heard and felt; it is then, however, pre-systolic. Like all murmurs of the same class, this is heard louder on the right than on the left side, because the interval between the heart and the cervical veins is shorter on the right, and consequently the veins on this side empty quicker. A murmur of regurgitation can be heard, too, in the cervical veins, after an aortic aneurism has opened into the superior vena cava. DISEASES OF THE ENDOCARDIUM. Historical Sketch. Literature: K. Sprengel, Versuch einer pragmatischen Geschichte der Arznei- kunde. Halle, 1803.—P. J. Philipp, Die Kenntniss von den Krankheiten des Herzens im 18. Jahrhundert. Berlin, 1856 — F. Martini, Beitrage zur Ge- schichte der Lehre vom Herzen und den Herzkrankheiten. Inaug. Diss. Berlin, 1869. It is self-evident, considering the scanty knowledge the an- cients had of the structure and functions of the heart, that va- rious phenomena, such as palpitations and syncope, although at- tracting their attention and observation, were never attributed to distinct cardiac affections. It was not till the sixteenth century, when post-mortem examinations had laid the general foundation of anatomy, that, after Vesalius' extensive investigations on the normal structure of the heart, and Harvey's brilliant discovery of the mechanism of the circulation, numerous pathological results roused a spirit of more accurate investigation. The progress made in the eighteenth century is astounding. First, Raymond Vieussens, who has enriched our knowledge of the anatomy of the heart, even more than its pathology, describes a case of stenosis of the left ostium, accompanied by insufficience of the mitral valve; and in his review he both gives it its proper significance and acutely explains the secondary hypertrophy of the ventricle, and the quality of the pulse which he had observed during life. He treats a case of aortic insufficiency in the same manner. His contemporary, John Maria Lancisi, drew attention to the dilatation of the right side of the heart, and simultaneous swelling and undulation of the cervical veins which accompany disturbances in the pulmonary circulation. Albertini estimated still more exactly the connection which exists between disturb- ances of the respiration and circulation, in consequence of 62 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. valvular defects. He too made use of and recommended the first physical method, namely, palpation of the cardiac impulse, for diagnosis of heart diseases. Morgagni, the inventive and bril- liant investigator in pathological anatomy, in four letters of his work, "De Sedibus," devoted to heart diseases, describes the mechanism of the disturbances which valvular defects produce, and even goes so far as to attribute the symptom of cyanosis solely to stagnation of the circulation. His work was greatly lightened by his contemporary, Senac, who first devoted himself to the systematic study of the diseases of the heart. Apart from numerous anatomical and physiological discoveries, which this investigator propagated, he was also the first to bring forward the influence of age as etiological, and mentioned cerebral affec- tions among the secondary symptoms or complications (as the case might be) which follow in the train of heart diseases. Cor- visart took a fresh step in advance, by adopting Auenbrugger's newly-discovered method of percussion, as a means of diagnosis in addition to palpation, which had already been practised by Albertini and Senac. By this means, as he assures us, he in gen- eral correctly estimated during life the circumference of the heart. Laennec, too, asserts that his teacher, Corvisart, was the first who recognized the fremissement cataire as a symptom of mitral affection. But neither he nor his predecessors were aware of the anatomical foundation of these valvular diseases. It was re- served for Kreisig to find this in the inflammation of the endo- cardium. He, in fact, has established the significance of all we see in the post-mortem examination with the naked eye. He also found that endocarditis was a frequent complication in the course of scarlatina and rheumatic arthritis. Bouillaud, how- ever, was the first to introduce the term "endocarditis," and must not be denied the merit of having laid more stress than others on the frequency of its occurrence in rheumatic arthritis, and of having recognized the disease during life. This latter he was enabled to accomplish by Laennec's discovery of auscul- tation. Though the immortal Laennec fell into occasional errors in interpreting the symptoms he discovered, still he is the originator of the method which alone enables us to diagnos- ticate a cardiac affection in the living subject. Among HISTORICAL SKETCH. 63 French and English observers, we should mention especially Andral (in his 4th edition of Laennec's Treatise), Piorry, Williams, Hope, and, above all, Corrigan, who put for- ward the oscillation theory, and who was the first to describe the physical signs of insufficiency of the aortic valves. Skoda and his school not only enlarged the limits of the physical signs of disease, and perfected the methods of ascertaining them, but they were also the first to point out what are the general con- ditions necessary for the production of certain symptoms. Kiwisch, Weber, Heynsius, Marey, Wolff, Landois, Chauveau, and others, have experimentally proved the physical conditions which produce the murmurs, and the different qualities of the pulse. The knowledge of pathological anatomy advanced hand in hand with the progress of diagnosis. We owe an exact insight into the normal and pathological anatomy of the endo- cardium and endocardial products to Luschka, Rokitansky, and Virchow. Virchow, in his works on embolus, has rendered the pathogenesis of the sequela3 of valvular affections susceptible of a mechanical explanation ; and he was also the first to acquaint us, in an accurate manner, with the anatomical changes which lie at the foundation of endocarditis. To Traube is due the credit of having first called attention to the important relations which subsist between the diseases of the heart and those of the kidneys. This investigator has enriched our knowledge of both the physiology and the pathology of the heart by an extensive series of important observations and experi- ments ; and he has also added to our knowledge of the thera- peutics of heart diseases, by his monographs on the action of digitalis. Stokes, Bamberger, Friedreich, Duchek, and von Dusch, by their excellent treatises and important investigations into details, have added materially to this department of medical science. Inflammations of the endocardium, according to their charac- ter, end either in ulcers, in thickenings of the membrane, or in villous formations of connective tissue, which in course undergo further changes. Corresponding to this, and with a view to the duration of the process, we shall divide them into 1. Acute ulcerative or diphtheritic endocarditis. 64 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. 2. Acute and subacute verrucose endocarditis. 3. Chronic sclerotic endocarditis. Acute Diphtheritic Endocarditis. Ulcerative Endocarditis. Literature : Besides the well-known text-books by Bamberger, Duchek, Friedreich, and von Dusch, consult W. S. Kirkes, in Edinb. Med. and Surg. Journal, 1853, Vol. XVIIL; and On ulcerative inflammation of the valves of the heart, etc., in Brit. Med. Journ., 1863.— Virchow, Gesammelte Abhandlungen, 1856, and second edit., 1862, from p. 505 on.—Bekmann, Ein Fall von capilliirer Embolie, in Virchow's Arch. 1857.— Ogle, On Ulcerations, etc., Transact, of Pathol. Soc., 1860.— Westphal, Endocarditis ulcerosa im Puerperium, Virch. Archiv, 1861.— Charcot et Vulpian, Note sur l'endocardite aigue ulcereuse, etc. Gazette mgd. 1862.—Lancereaux, Recherches cliniques pour servir a" l'histoire de l'endoc. suppuree, Gaz. Med. 1862.—Schivardi, De l'endocardite ulcereuse. Union med. 1865.—Herard, Endocardite ulcereuse. Archiv. gentir. 1865.—Moxon, Case of ulcer, endoc. of the right heart, in Transact, of Path. Soc, Vols. XXI. and XIX. — Whipham, A case of jileurisy with hemothorax complicated by ulceration of the tricuspid valve. Ibid. Vol. XX.—Tuckwell, Endocard. with embolism. Ibid. —Aufrecht, in P. Niemeyer's Handbuch der Percussion, 1868, p. 151.—Bumken, Die ulcerose Endocarditis. Berlin, 1868.—Oppolzer's Lectures, Ueber die ulce- rose Form der acuter Endoc. Allgem. Wiener Med. Zeit. 1868, Nos. 14 and 16.— Rudolph Meier, Ueber die Endocarditis ulcerosa. Zurich, 1870.— Virchow, Ueber Chlorose, etc., insbesondere iiber puerperale Endocarditis. Berlin, 1872.— Heiberg, Ein Fall von Endoc. ulcerosa, in Virch. Archiv, 1873, and Die puer- peralen und pyamischen Processe. Leipzig, 1873.—Lancereaux, De l'endocar- dite vegetante ulcereuse et de ses rapports avec l'intoxication palustre. Arch. gener. 187S.—Eberth, Ueber diphtheritische Endocarditis. Virch. Arch. Bd. 57.— Burkart, Ein Fall von Pilzembolie. Berliner klin. Wochenschr. 1874. No. 13.—C. Eisenlohr, Ein Fall von Endocarditis ulcerosa. Berl. klin. Wochenschr. 1874, No. 32.— Rudolph Meier, Ein Fall von primarer Endocar- ditis diphtheritica, in Virchow's Arch. Bd. 62. Heft 2. It is only in modern times that searching attention has been bestowed on that form of endocarditis which is distinguished no less by its acute, malignant course, than by its peculiar ana- tomical product. The fact that it is always accompanied by ulcers, distinguishes it indeed from the verrucose or vegetative and the sclerotic forms, which occur more frequently, but still does not fully express its qualities, as there are many benign "losses of substance," which only form slowly and by degrees on ACUTE DIPHTHERITIC ENDOCARDITIS. G5 the endocardium ; the latter appear to belong more to the fatty consumption we meet with in endoarteritis. The malignant nature which characterizes this affection is not to be attributed simply to the ulcerative process, but to the peculiar fundamental disease which induces the ulceration. Virchow, who was the first to investigate the pathological changes somewhat accurately, and whose description we shall follow, called attention, even in his first communications, to the similarity of this process to that which takes place in diphtheria ; and all recent investigations tend more and more decidedly to confirm this view. Hence, it appears more correct to adopt the term "diphtheritic" than '' ulcerative '' endocarditis. Anatomical Appearances.—The usual seat of diphtheritic en- docarditis is in the left side of the heart. Both the mitral valve (especially the tip of the anterior flap), and also the flaps of the aortic valves, are most frequently affected. We next find it, in order of frequency of occurrence, on the walls of the auricular ap- pendices (especially of the left auricle) and of the ventricles. On the tricuspid and pulmonary valves it occurs only exceptionally, but still this has been repeatedly observed. Whipham, for in- stance, describes a case (Path. Transact., 1871), where the disease was confined to the tricuspid valve alone ; while similar observa- tions have been twice made on the pulmonary valves. As oc- curs in the course of inflammation in other vessels, so here also the first stage is hyperemia of the vessels which supply the intermediate layers of connective tissue. There is as little proof for this derived from actual observation as there is for the sup- position that an exudation is poured on to the free surface of the endocardium, which is washed away by the circulating blood. The occurrence of parenchymatous changes in the tissue at the very beginning of the disease has been firmly established. The cellular elements absorb material till they enlarge, swell, and are rendered non-transparent by their granular contents. From the very commencement the affected parts of the endocardium appear of a dirty gray color, opaque and dull, but still there is no trace of unevenness visible to the naked eye. Very soon, however, when the proliferation in the connective-tissue nuclei of the elastic reticular fibres grows more active, granulations of VOL. VI.—5 66 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. various size are formed. Simultaneously those surfaces which have lost their brightness and smoothness become the seat of fibrous deposits, and these organize themselves into a felt-like mass with the underlying tissue. The tissue itself has grown loose, and can be easily torn away. The small granulations and the fibrinous deposits on these crumble away, the tissue softens, and an ulcer is formed, on and around which the stream of blood is continually depositing fresh fibrin. Actual formation of pus, consequently, seldom takes place, being generally anticipated by the dissolution of the tissue; it is only in rare cases that abscesses have been observed, whether in the connective tissue which unites the two layers of the valvular reduplication, or whether it be in between endo- and myo-cardium. This has been the experience of Lancereaux in particular. The usual result we find is a perforated valvular surface; this is surrounded by excrescences, and is uneven, felted, ulcerated, or even covered by a bleached coagulation. In other cases, which come under observation in an early stage, we see little more than yellowish spots, or a dirty gray patch of a few millimetres in thickness, and around it a swollen and dull endocardium; nor can we remove it from its position without loss of substance. If we accurately examine the dulness occurring in spots, or the more diffuse patch, or the substance which is found on the ulcerated place itself, they will all be found to consist of "the most various-shaped granular particles," as Virchow so happity describes them; and these bear the greatest re- semblance to diphtheritic formations. It forms a very finely granulated mass, almost a detritus, which microchemically dis- plays a strong resistance both to acids and to alkalies. These fine granules have often been held for fat globules, but treat- ment with alcohol or ether shows the groundlessness of this view. In a small but well attested series of cases these sub- stances have been proved with certainty to consist of parasitic organisms of the micrococcus genus (Winge, Heiberg, Burkhart, Eisenlohr). Virchow himself has confirmed this result in the case of Heiberg's specimens. And in this we have further grounds for retaining our view of this pathological product as diphtheritic in the anatomical sense. On the affected parts of ACUTE DIPHTHERITIC ENDOCARDITIS. 67 the endocardium, especially on the valves, the ulcerated condi- tion of the membrane, and its mode of origin, can give rise to further changes, both in the valves themselves and also in dis- tant organs. The looser and more easily torn the tissue becomes, so much the easier can a lamella of a valve tear, even before ulceration has set in, and then the lamellae, which remain unin- jured, are stretched and bulged out by the strain of the circula- tion. This occurs still readier when ulceration has already de- stroyed one lamella, and in this manner are formed the so-called acute valvular aneurisms, convexities varying in size from a pea to a bean, or a walnut; they arise on the auriculo-ventricular valves, and project into the auricles, or on the semi-lunar valves and project into the ventricles. The bottom of one of these aneu- rismal sacs may be perforated, and the ragged edges of the open- ing produced may form a source for embolic processes. An aneurism of this kind, especially by depositing large thrombic masses, can build a considerable tumor, and in this way lead to acute stenosis of the ostium. Still the majority of acute insuffi- ciencies are produced by spreading of the ulceration to the base of the flap, which is thus loosened and destroyed, or, if the process spreads in the other direction over the chordae tendinae, by dragging these away. When the ulceration is localized in the ventricles instead of on the valves, then the pressure of the blood drives out the cardiac wall ; and this, when complicated with myocarditis, may give rise to a so-called partial cardiac aneurism. Communications of all kinds, too, are formed accord- ing to the situation of the ulceration ; thus a communication between the two ventricles has been observed, resulting from ulceration of the septum. In another case we see communica- tion of this kind taking place between the right auricle and the anterior wall of the aorta. If the disease be located in the left side of the heart, and if small particles of the crumbling parts, or—more rarely—large shreds of tissue be swept onward by the current of the blood, and enter the circulation of those organs which possess—as Cohnheim's investigations have shown —" terminal arteries" and valveless veins (as is the case, e. g., in the spleen, kidney, brain and eye), they will give rise in these organs to infarctions, by inducing secondary changes in the cir- 68 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. dilation. Where the tricuspid valves are diseased, or where- thrombi have formed in the right side of the heart, or, finally, where there is coincident thrombosis of peripheral veins, infarctions, or—still oftener—abscesses from embolism, will also be found in the lungs, which possess "functional terminal arteries." Abscesses from embolism may form in all the organs of the body, for, as Cohnheim has shown, the embolus acts in these organs merely the part of an infective exciter of inflam- mation. It is an extremely interesting fact that organisms, which are now unanimously accepted as parasitic, have been found by Virchow, Bekman, von Recklinghausen and others, in the seats of metastasis, in the afferent vessels of the above- mentioned organs, and that these organisms are similar to those which occur also on the original focus of the embolus. We must here mention a peculiarity of the acute malignant form, which distinguishes it from the subacute verrucose, namely, the acute form but seldom leads to large clots, while in the great majority of cases it produces multiple, capillary emboli. A peculiar property of these emboli is that they not only cause mechanical obstruction, but they also act as a chemical infec- tant, and are thus, in themselves, the symptom of a general blood poisoning, or else lead directly to this result. In spite of the certainty which some authors express, that the changes in the skin and mucous membranes, so often occurring in the course of endocarditis, and especially the capillary extravasa- tions which we find almost without exception on the mucous and serous membranes, together with the pustulous exanthe- mata of less frequent occurrence, depend upon embolical pro- cesses, the question is still undecided. Embolic obstruction has as yet been proved in very few cases, and it is quite possi- ble that here, as on other occasions where infection is involved, changes in the walls of the vessels, perhaps only of a functional nature, may render them more liable to rupture. The character of universal infection is also displayed in the coarse parenchy- matous alterations in the glandular organs of the abdomen and in the myocardium, and the case is not affected, whether we assume an inflammatory origin for these, or whether we regard them as the expression of deficient nourishment. The spleen ACUTE DIPHTHERITIC ENDOCARDITIS. 69 is always found enlarged, often to twice its normal size, even in cases where no infarction has occurred ; the liver is sometimes of the normal size, but generally hypertrophied, and only exceptionally atrophied; this last result, however, can sel- dom, with certainty, be attributed to endocarditis. In the kid- neys we meet with stripes of miliary, so-called "abscess for- mations," and these obstruct the afferent vessels with parasitic organisms. Similar clots, too, occur in the uriniferous tubules and vessels of the glomeruli, even in cases where the bladder and ureters are perfectly intact. Hardly a single case occurs without changes in the epithelium. The brain still remains to be mentioned in the category of distant organs, which display pathological results that are directly attributable to endocarditis. Extravasations into the meninges have been repeatedly observed, sometimes confined to the surface, and at other times piercing deeper, occasionally into the cerebral substance itself. But embolical obstructions of the larger vessels, and metastatic abscesses do not occur here so frequently in this class of endocarditis. On the heart itself we find pericarditis and myocarditis (the latter more frequently), either directly produced from the endocarditic centre, or brought about by emboli in the coronary arteries. The changes affecting the lungs are generally the result of emboli from the right side of the heart, and assume the form of metastatic abscesses; this has been several times observed to produce pleuritis, and in one case actually haemo- thorax. In isolated cases, as in the one observed by Herard and Sander, there was no indication whatsoever, either of an abscess or of secondary infarction. About the changes the blood itself undergoes in this severe general disease, nothing is known. Virchow has indeed made one observation, where he found, two days after the death of the patient, that the blood had an acid reaction, and when boiled, precipitated tyrosine and leu- cine ; but then we must by no means forget that these changes were observed post-mortem. 70 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Etiology. Here we must distinguish between a primary and a secondary form. For the first we know absolutely nothing causal in the sense of a necessary connection between cause and effect. We have only learned empirically some pathological condi- tions for it, which usually precede the development of diph- theritis, and on account of this we feel bound to assume some allied cause for both. The disease, however, seldom attacks perfectly healthy people. In the great majority of cases it has been observed in the course of acute rheumatism, seemingly unaffected by the number of joints attacked or the degree of pain. The cardiac disease does not usually commence till that of the joints has run on for some days ; and after the fever has begun to give way, a severe shivering fit ushers in the endocar- ditis. The form which occurs during puerperal fever represents a transition stage from the primary to the secondary. Though in some cases we can find no symptoms of disease on the geni- talia, yet in others the most undoubted diphtheritic affections have been seen on the mucous membrane of the uterus or vagina. And in these very cases the likeness between the diphtheritic matter found on the genitalia and that which covers the endocardial abscess, is so strong, and parasitic organisms have been detected with such certainty in both cases, that noth- ing but the most stubborn incredulity could deny a connection, brought about by the blood, between the affection of the geni- talia and the endocardial centre. We do not wish, however enticing it may be, to make any conjectures as to the part which parasites play in these cases as the exciting causes of disease ; still we must be allowed to consider them as the con- necting agent between the puerperal affection of the uterus, etc., and the endocardial process. The same holds good for another series of diseases arising from wounds, where the wounds (whether external, as in Winge's case, or internal [fausse route], as Eisenlohr observed) are the primary seat of the disease, and the endocarditis only a secondary affection, or, in other words, where the ulcerative endocarditis is only a part ACUTE DIPHTHERITIC ENDOCARDITIS. 71 symptom of the presence of pyo-septhaemia. We should be undoubtedly justified in regarding the colonies of micrococci, which are also to be found here, as the real cause of the endo- cardial disease, and in looking upon the whole as parasitic, if it were not that on the one hand observations have been recorded, where no thought of such a connection can be entertained, and that on the other hand even cases of puerperal ulcerative endo- carditis itself have been observed where no other etiological factor could be brought forward besides the usual rheumatic one due to cold caught during perspiration. Besides this, the verru- cose form of endocarditis occurs in rheumatic arthritis, and in puerperal fever, too, oftener than the ulcerative. Thus, though the ground process of the two is the same, yet a disposition to disease appears to exist in the endocardium, which, under cir- cumstances as yet unknown, presents itself in the ulcerative form. As regards the defective development of the vessels, which Virchow has urged, and the existence of which he has only proved in a few cases, it remains to be decided how far it can be regarded as a material ground for a so-called predispo- sition. In any case, from the fact that old valvular defects can only be regarded as etiological in the third degree, we can imagine how much importance should be attributed to previous vascular changes. Several of the observations already made (and to which I can add one of my own) prove that previously existing old endocardial changes, in particular a thickened and retracted tissue, which so frequently dispose to recrudescent verrucose inflammations, may occasionally form a favorable ground for the development of an acute ulcerous process. It is extremely doubtful whether we may reckon typhoid and acute typhus as etiological. Rudolph Meier has called atten- tion to the fact that in the one case which Griesinger adduced to prove this assumption, and in which endocarditis followed typhoid, there is no evidence to prove whether this was the ulcerative form or not; and the female, on whom Vast observed ulcerative endocarditis after measles, had previously suffered from rheumatic arthritis. It is still less justifiable to bring forward acute or chronic diffuse nephritis in any causal relation to diphtheritic endocar- 72 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. ditis. Out of the numbers of persons affected with renal dis- ease, who have come under my notice, I have never seen one with this cardiac complication; and even if one such case is described, we still have no right to promote such an exception to the etiological paradigm. Age alone remains to be mentioned among the circumstances whose influence we have empirically learned. In the majority of cases observed the patients were young, under thirty years of age ; only a few were over forty. The first case on record, which is described by Senhouse Kirkes, was a boy of fourteen. Sex and occupation have not as yet been observed to exert any influence. Symptoms. It would be impossible to draw a tabulated general de- scription applicable to every case of endocarditis, since hardly two cases have been found exactly alike. We can only con- struct certain types by abstraction from the observations at our disposal, and arrange the different phenomena under these, so as to form a harmonious whole. The types, two in number, are the typhoid and the pyemic. The prevailing symptoms in the typhoid form are the general constitutional disturbance and the nervous disturbances, which produce the same impression on the observer as typhoid fever ; in the pyaemic form the character of the fever and the occurrence of the various metastases con- stitute the distinguishing characteristics. However, many cases fall distinctly under neither the one head nor the other. The following is a general outline of the typhoid form. 'After the patient has been complaining for some days of more or less sharp pains in the joints, these give way, but the accompanying fever remains either very high, or, if it has gone down, a severe shivering fit comes on suddenly, and is followed by heat and perspiration. Defined local complaints, which would call the physician's attention to the heart, are seldom made, even though the disease be complicated by pericarditis; the patient only complains of headache, giddiness, general prostration, and some- times of an oppressive feeling of pressure in the epigastrium. ACUTE DIPHTHERITIC ENDOCARDITIS. 73 The temperature generally remains high, but varies too between a remittent and an intermittent character ; the pulse is quick, soft, and small ; the tongue is dry; the lips are covered with a sooty coating; vomiting comes on, sometimes only at the beginning, other times repeatedly all through the course of the disease; diarrhoea and constipation succeed one another ; the abdomen is puffed up, and the spleen swollen. The patient is at first col- lected, but becomes confused; delirium and somnolence succeed one another, till the latter reaches the stage of perfect coma. Urine and faeces are involuntarily passed; the urine is dark, and contains albumen and sometimes blood. The objective examina- tion of the different organs shows that the spleen is enlarged and painful on pressure. Over the heart we usually hear a loud systolic murmur, occasionally a diastolic one; sometimes it is best heard over the apex, sometimes over the base, but especially in the neighborhood of the aortic ostium. Whether we find an extension of the cardiac dulness to the right or left, or whether there are, as usually occurs, no changes at all in the cardiac volume, all depends upon the situation and area the process has taken up. Complication with pericarditis can produce very con- siderable changes in the physical symptoms. The commencement of the pyemic form also announces itself by a severe shivering fit. The fits then recur, either with perfect irregularity, several times in a day, or sometimes with such per- fect regularity of paroxysm and apyrexia that the observer would at first imagine he had an intermittent fever before him. A lying-in patient may have left her bed after the puerperium, and feel apparently perfectly well, when the first attack of shiv- ering, followed by considerable depression and general prostra- tion, announces the arrival of endocarditis. In addition to the general disturbance of the system, here strikingly developed, and to the peculiar course of the fever, metastases occur in this form with great frequency, though we are incapable of detecting most of them during life. Amongst the first occur roseolar, petechial, or hemorrhagic spots on the skin, or even a rapidly- developing pustulous exanthema, calculated to attract attention. In other cases we see a jaundice-like coloring of the skin and conjunctiva. Diarrhcea is frequently observed, and blood is 74 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. generally mixed with the stool. A swollen spleen and albumen in the urine occur in almost every case. The local phenomena in the cardiac region are similar to those in the typhoid form. In both the patients are generally unconscious before death takes place. But besides these pretty sharply-defined forms, intermediate ones occur, isolated cases, which give us the impression that we only have a rheumatic fever to deal with. Even the most accurate objective examination can detect no physical symptoms of the local disease. Vague feeling of pain in the joints and muscles, accompanied by a fever, with its temperature curve belonging to no special type, but keeping on the whole pretty high, and with a rather rapid pulse—these, and some corresponding gastric dis- turbances, are the only signs of the disease, in its course quite as destructive as the others. When, in order to become better acquainted with the varia- tions, we consider the symptoms one by one, we meet with the following: The local appearances in the cardiac region, which we should be inclined to rank first, on account of their diagnostic value, are by no means always clearly expressed. Subjective com- plaints are rarely made; there was no pain when the case was not complicated by pericarditis. Some had a feeling of dread and oppression, others had none. The most frequent cause of trouble was the sensation of palpitations of the heart. The objective examination, too, left a great deal unexplained. It is quite comprehensible that there is no ground for the production of murmurs, and that we do not hear them when the endocar- dial changes are located on the walls of the ventricles and auri- cles. But even in cases where the valves are the seat of the disease, there may be no murmur audible, not only before ulceration has actually taken place, but even—as has been ascer- tained beyond a doubt—during the entire progress of the ulcera- tive process. In the majority of cases, however, that ambiguous sign, a systolic blowing sound, occurs quite early in the course. Signs of hypertrophy of the heart and stagnation in the pul- monary circulation soon succeed, when the progress of ulceration has produced an acute incapability of closure of the valves, by ACUTE DIPHTHERITIC ENDOCARDITIS. 75 loosening off a flap, or by perforation. The duration of the whole process is generally too short to admit of any very mani- fest development of secondary changes, and it may be laid down as a general rule that we never find an enlarged area of dulness unless chronic valvular disease is present or a fresh pericardial exudation has taken place. Diastolic murmurs, too, are heard when the disease is confined exclusively or in greater part to the aortic valves, while these murmurs are scarcely ever heard when the mitral valve is affected. Respiratory disturbances are observable in many cases, and are rendered remarkable by the discrepancy between the sub- jective dyspnoea, and the few changes we can discover in the lungs. Obstruction of the circulation in the pulmonary vessels is generally the cause of the shortness of breath. It is only in exceptional cases that the stagnation is so great as to produce ruptures in the vessels of the bronchial mucous membrane and haemoptysis. AVhen the tricuspid valves are diseased, or when there is thrombosis of the right side of the heart, or when, finally, there are thrombi of the peripheral veins, the signs of haemorrhagic infarction, with or without secondary pleuritis, will also be observed in the lungs. When no marked changes are to be detected in the lungs or pleura, we must not forget that the respiratory difficulties can be due to the presence of pericarditis. The changes in the system in general, especially fever, are far more constant than the cardiac phenomena. Fever, though oc- curring under different forms, is never absent. Most frequently it assumes somewhat the temperature curve of an irregular inter- mittent. Especially at the commencement abnormally high tem- peratures of 105.8° F. (41° O), and higher, fall in twenty-four hours, or in several days, to or below the normal. This increase of warmth is generally connected with the feeling of a cold shiver, and followed by heat and perspiration. But at the com- mencement intervals of apyrexia occur, in alternation with high temperatures. But in the succeeding course the character of a febris remittens or subcontinua is generally assumed, though shivering fits often recur; towards the end of the disease these 76 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. fits cease altogether. In isolated cases, highly important from their easy confusion with ileo-typhoid, the initial shivering fit is the only one which occurs during the whole course, and the fever assumes a subcontinuous remittent character, with an evening temperature of from 104° to 105.8° F. (40°—41° C), and a morn- ing one of 102° or 103° F. (38.8°—39.2° C). In one case of this nature I repeatedly found the so-called "inverse type," or a higher temperature in the morning than in the evening. The pulse has always been observed as abnormally frequent, and, especially if the case is complicated by myocarditis, it reaches to extraordinarily high numbers. It is not marked by any further peculiarity, and when sharply defined abnormalities in its fulness or rhythm occur, pericarditis or myocarditis is present as well, and should be regarded as the cause. Disturbances in the digestive organs, as vomiting or diarrhcea, occurred in almost every case, and especially in some observed by Lancereaux, their intensity was so great, and threw every- thing else so completely into the shade, that at first they gave him the impression of cholera. Vomiting, however, generally occurs only at the beginning, while diarrhoea and meteorismus accompany the whole course ; constipation, on the contrary, is seldom observed. In some cases, pathologico-anatomical causes, such as intestinal catarrh, swelling of the follicles, etc., have been detected as the foundation of these functional disturbances ; especially when blood has been passed with the faeces, embolical masses have been found in the branches of the mesenteric artery. But frequently we can find no anatomical changes, and the in- testinal phenomena, particularly vomiting, must be regarded as symptoms of infection ; similar phenomena may be experi- mentally shown on animals after the introduction of putrid mat- ter ; they occur, too, as forerunners of acute exanthemata, and this is especially true of the vomiting. For other disturbances, even for some gastric ones, we must take into account the changes which take place as well in the glandular organs of the abdomen as in the alimentary canal. Of these glands, the liver is the one most frequently affected. Mere epithelial changes, when they do not extend to dissolution, produce no striking re- sult. In one case observed by Schnitzler, marked atrophy of the ACUTE DIPHTHERITIC ENDOCARDITIS. 77 parenchyma took place, and was accompanied by icterus. In two other cases where icterus was present, emboli were found in the branches of the hepatic artery. In most cases which were complicated by jaundice, nothing material could be found to ac- count for the symptom. The capillary gall-ducts, indeed, were never examined. The spleen could generally be recognized during life as en- larged, and was often accessible to palpation. The tension on its serous membrane explains the sensation of pain the patient experienced from percussion, and which often occurred without external cause. Disturbances in the diuresis are mostly to be recognized as abnormal constituents in the urine. Parenchymatous changes in the epithelium, and the changes in the circulation brought about by the fever, are the principal causes of albuminuria. The occurrence of haematuria is very rare, and is only brought about by the infarction of very large clots; metastatic miliary abscesses give us hardly any external symptoms. The phenomena exhibited in the nervous system relate chiefly to the sensorium, and display at first an irritant character, but depression very soon succeeds. The symptoms of irritation have never been observed to increase to continuous puerperal mania, except in one case described by Westphal; but this patient had formerly suffered from mental disease; and Rudolph Meier is certainly right in considering this one case as insufficient evidence to establish a causal nexus between ulcerative endo- carditis and acute mental disease. It is impossible to say positively how far the deleterious influence of an abnormally high temperature is concerned in the production of the states of irritation and depression in the sensorium. But this much is perfectly certain, that this cause can be assigned only in a very limited number of cases, since most of the nervous disturbances occur right at the beginning of the disease. So in this case, as in typhoid and acute typhus, we must consider the phenomena as dependent on the action of abnormally constituted blood on the nervous centre, until more apparent anatomical changes can be found on which we may lay a material foundation. The cortical substance of the brain has been very seldom examined in these 78 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. cases, though occasionally embolic obstructions have been found in the capillaries. In addition to the sensorial disturbances, we often meet with paralysis, generally as hemiplegia, with well- defined central origin. These cases always resulted from coarse lesions in and on the brain, such as blood extravasated into the cerebral membranes, on and between the gyri, and even pressing into the substance of the brain, or else soft patches resulting from embolical stoppages in the arteries of the Sylvian fissure. Where the optical functions were affected, the cause was found to lie in extravasations in the choroid or retina, or in inflammation of the whole eye, resulting from obstruction in the branches of the ophthalmic artery. Diagnosis. Diphtheritic endocarditis can seldom be diagnosticated with certainty, and is generally either altogether overlooked, or at most conjectured. This is not surprising, considering how little the complaints of the patient attract attention to the local disease, and how ambiguous both the local and general symp- toms are. In fact, there are no local symptoms at all, unless the disease be seated on the valvular apparatus. Even in this case a systolic murmur has no special significance, as it may be of a quite accidental nature. A diastolic murmur would be of more value ; but to estimate it properly, we must exclude the existence of a chronic heart disease. As a matter of fact, the mere presence of these auscultatory phenomena is not of so much diagnostic value as the changes in their character. The earlier observers, and especially Charcot and Vulpian, have pointed out the worth of this, showing that according to the de- gree and progress of the ulceration, at first only a systolic blow- ing sound is heard, confined to the area of the apex, which next grows weaker here and more audible over the base ; afterwards it is complicated with a diastolic blowing sound, and finally exhibits all the signs of perfect insufficience ; they showed, in a word, that the auscultatory sounds go through a number of stages. The symptoms of enlarged area of superficial and deep- seated dulness occur when we have acute valvular insufficiency. ACUTE DIPHTHERITIC ENDOCARDITIS. 79 and seldom under any other circumstances, except it happen that pericarditis too is present. When such a combination of auscultatory and percussional symptoms takes place under our eyes, the diagnosis of endocarditis in general is an easy matter, and consideration of the general state of the system and the etiology (should we be able to ascertain it) will establish its diph- theritic character. But if, as is usually the case, we find the local appearances indistinctly marked, the general state of the system is more likely than anything else to lead us to confusing it with typhoid fever, irregular intermittent fever, or some other pathological state. Confusion with intermittent fever may be easily avoided, since no genuine apyretic intervals occur in endocarditis, at least only in the very beginning, and later on mere remissions ; besides, the shivering fits occur unaccompanied by any decided change of temperature. But ulcerative endo- carditis can simulate typhoid much more closely, for the spleen is nearly always enlarged, and a roseolar or petechial exanthema is very often present, and frequently accompanied by meteoris- mus. However, the striking disproportion in the duration of the disease, and the severity of its symptoms, as well as the absence of the temperature curve so peculiar to typhoid, and the abnor- mal rate of the pulse, will all suffice at least to establish a well- founded doubt of its typhoid character. But the most important point is the consideration of its etiology, such as rheumatic arth- ritis, puerperium, chronic valvular disease, pyaemia, and trau- matic diseases in general. When one of these etiological factors is present, and the local and general symptoms which we have mentioned occur on its foundation, the probability of the diag- nosis is greatly strengthened. It becomes a matter of certainty in those cases where embolical processes, which are easily de- tected, occur simultaneously (e. g., development of panophthal- mitis purulenta, hemiplegia, etc.), and where we can exclude all sources of emboli other than the cardiac valves, and likewise any chronic valve disease. Duration. The scantiness of the material which has come under observa- tion renders the calculation of its duration very difficult, and, 80 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. besides, the commencement of the disease is often not exactly defined. The cases which occurred after rheumatic arthritis lasted from two to four weeks, while those which came on in the course of pyaemia and during the puerperium ended fatally in a far shorter time, sometimes in from four to six days. Spontane- ous cases, and those where the valvular disease is recurrent, last comparatively the longest. Prognosis. From an anatomical point of view, recovery is not impossible, especially when the process has not gone beyond its first stages. And even if an ulcer do form, it may heal to a scar, and thus recovery set in, if general infection was not the result or the origin of the endocardial disease. As a matter of fact, however, there is no case of recovery on record, and after the diagnosis has been once firmly established, the prognosis must be regarded as extremely unfavorable. Treatment. Though we can easily establish indications, our present means are not capable of meeting them. A genetic treatment is perhaps most admissible in cases of puerperal diphtheritis and traumatic pyaemia in general. Yet here the local treat- ment is too feeble to ward off the spreading of pyaemia. Besides the regulation of a favorable diet, when possible, our only re- sources are the lowering of the excited activity of the heart and the reduction of the fever. In regard to the former, the local application of cold in the shape of ice-bags is the most pref- erable. With this may be connected the internal use of mineral acids, which lower the action of the heart, and have a long- standing repute as antiseptics. To combat the fever, quinine in large doses is indicated. The use of salicylic acid seems espe- cially suited to cases where there is some probability of a parasitic origin of the disease. Digitalis, such a sovereign remedy in all other heart diseases, must be employed here with the greatest caution, since further gastric disturbance and weakening of the SUBACUTE VERRUCOSE ENDOCARDITIS. 81 heart's action are greatly to be feared. If this latter occurs, it must be met with such well-known stimulants as camphor, carbonate of ammonia, musk, etc. Friedreich, on account of the relatively successful results he professes to have obtained, recommends the further trial of corrosive sublimate. It seems to me worth while to make further trial of Lender's method of inhaling ozone for pyaemic cases. Acute and Subacute Verrucose Endocarditis. In addition to the works mentioned in the preceding paragraph, compare: F. L. Kreyssig, Die Krankheiten des Herzens. Vol. II.—Bouillaud, Nouvelles recher- ches sur le rheumatisme aigu en general et specialement sur la loi de la coin- cidence de pericardite et de l'endocardite avec cette maladie. Paris, 1836 ; and Traite clinique des maladies du cceur. Vol. II. pp. 1-150.—Franz Zehetmayer, Die Herzkrankheiten. Wien, 1848, p. 232.—Luschka, Das Endocardium und die Endocarditis, in Virch. Arch. Bd. IV.; and Ueber zottenformige Bildungen an den Semilunarklappen der Aorta, Deutsche Klinik, 1856.—Ruhle, Ueber Herzkrankheiten, in Giinsburg's Zeitschrift, 1852.—Rokitansky, Ueber das Auswachsen der Bindegewebssubstanzen. Sitzungsber. der Wiener k. Acad. der Wissenschaften. 1854.—R. Virchow, Gesammelte Abhandlungen, p. 505, etc.—Richardson, The cause of the coagulation of the blood. London, 1858, pp. 371, etseq.—Mbller, Die Milchsauretheorie des Rheumatismus. Konigsb. Jahrb. 1860.—G. Reyhcr, Zur Frage der Erzeugung der Endocarditis, in Virchow's Archiv, Bd. 21, 1861.—Rauch, Ueber den Einfluss der Milchsaure auf das En- docardium. Dorpat, 1860.—Ileschl, Zur Casuistik und Aetiologie der Endo- carditis, in Oesterreichischer Zeitschr. fiir prakt. Heilkunde, 1862.—Aug. Olivier, Nouvelle note sur l'endocardite, etc., in Gazette medicale de Paris, 1862, p. 360, etc.—VEpine, Sur le siege de predilection de l'endocardite et de l'endopericardite d'apres de nombreuses observations. Gaz. med. deLyon, 1867. —Desnos et Hachard, Des complications cardiaques de la variole. Paris, 1871. —Labadie-Lagrave, Des complications cardiaque du croup et de la diphthene. Paris, 1873.—Rene Blache, Essai sur les maladies du cceur chez les enfants. Paris, 1869.—Paid Sperling, Ueber Embolien bei Endocarditis. Berlin, 1872. Inaug. Dissert. Pathological Anatomy. The subacute form of endocarditis, which supplies the tran- sition stage to the chronic, has many points in common with the latter. It occurs far more frequently than the diph- VOL. VI.—6 82 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. theritic. In extra-uterine life the subacute form is even more confined than the diphtheritic to the cardiac valvular apparatus of the left side, and to the chordae tendinae. Sperling, from the material of the Berlin Pathological Institution, gives a good esti- mate of the subacute and chronic forms of endocarditis in adults as regards their relative frequency of localization in the right and left sides of the heart. According to this, he found, out of 300 cases of endocarditis, 297 in the left side and 32 in the right; confined to the left side alone 268, and confined to the right alone 3, and simultaneously in both 29. In the foetus and new- born child the reverse held good. Rauchf uss, in St. Petersburg, found during his investigations 192 cases of fcetal endocarditis in the right side and 15 in the left. Those surfaces of the valve which face the current so as to encounter the greatest mechanical tension and friction, especially the lines of closure of the auriculo- ventricular valves, and the surroundings of the noduli Arantii on the semi-lunar valves, are the favorite seats of disease. Next to these in frequency we see it occur on the chordae tendinae, but relatively seldom on the endocardial lining of the ventricles. We find the posterior wall of the left auricle perhaps as fre- quently affected, according to L'Epine's estimate, more fre- quently ; but I may be allowed to remark that his calculations apply more to opacities and thickenings in general, than spe- cially to verrucose endocarditis. In the adult, too, the tricuspid, and even the flaps of the pulmonary valves, are only affected in very exceptional cases. With a view to express the relative frequency with which the affection attacks the different valves, Sperling tabulated Virchow's material, so that out of 300 cases of endocarditis he found it 255 times on the mitral, 129 on the aortic valves, 29 on the tricuspid, and 3 times on the pul- monary valves. In 157 cases the mitral alone was affected, in 40 the aortic valves alone, and the tricuspid alone in 3 cases, while the valves of the pulmonary artery were not the only affected parts in a single case. The verrucose products, which even Laen- nec regarded as purely fibrinous formations, are not the result of an organized exudation on a free surface, but the fruit of in- flammatory changes in the parenchyma. In the diphtheritic form we saw how the proliferation of young cells hastened the apti- SUBACUTE VERRUCOSE ENDOCARDITIS. 83 tude to tear and general dissolution of the tissue with enormous rapidity. But, in the present case, the most foremost changes are of a progressive and more enduring order, produced by an irritation, which, though not so virulent, lasts very much longer. The connective-tissue elements proliferate to form a jelly-like mucous tissue on the free surface and between the cells. The longer the process lasts, so much the firmer becomes its consist- ency, and so much the more numerous are the various excres- cences it forms. These latter vary, from the hardly perceptible velvet coating on the normally smooth valvular surfaces, to more or less opacity and swelling of the opaque spots, connected with wart-like, papillose, or even knotty and cauliflower-shaped out- growths in the form of a cock's comb, generally of a red or gray- red color, and always firm at the base, though the point may only have a jelly-like consistency. Fibrin is precipitated from the blood on the raw and projecting surfaces, and the fibrin becomes so entangled in the connective-tissue outgrowth that it is hard to separate the verrucose and thrombotic masses from one another, so much so indeed, that before Rokitansky's and Virchow's in- vestigations almost general ignorance of the histological nature of these products prevailed. The great likeness these small cock's comb papillae bore to epidermal excrescences and pointed condylomata led Corvisart to regard them as syphilitic. This view, though confirmed in one case (Julia), is incorrect for the majority. These polypous formations sometimes take up a more considerable area, and are sometimes even pedunculated and exhibit a certain degree of motion. It is chiefly in the aortic valves that we find these long tufts, swinging on threadlike stalks, and hanging into the ventricles. Where such pedunculated outgrowths came under my observation and had produced very plain symptoms during life, the cases had all run either a subacute or chronic course, not at all confirming Fuller's suppo- sition that they are always very rapidly formed. The chorda? tendinae may undergo the same changes as the valves, so that they come to look exactly like an ear of corn, and form the seat of thrombotic depositions. Whenever these latter occur, whether it be on alreadv formed excrescences, or on parts of the endocardium which are still in the raw stage, or 84 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. whether it be as "cardiac polyps," which often accompany endo- carditis as coagulations in the auricles or ventricles—in any of these cases there is a possibility of embolical processes taking place, and this possibility is realized in this form of inflammation through the agency of the most varied causes. But the very nature of the emboli, and their manner of occurrence, dis- tinguish the diphtheritic from the verrucose endocarditis. In the diphtheritic the size and number of the destructive metas- tases are in no way related to the area over which the ulceration has extended, while in the verrucose form metastases never occur except when large quantities of fibrin are deposited, and the clots block up larger arteries ; but they are fewer in number, and their action is mechanical and not infectious in most cases. Thus we can more accurately follow all the transformations in an embolus of this kind, such as filling with fat, calcification, etc. According to Sperling's statistics, the kidneys are the organs most liable to infarction, and not, as was generally sup- posed, the spleen. When the right side of the heart is affected, infarction takes place in the lungs, more particularly in the inferior lobes and especially those of the right lung. The Berlin material exhibited the following relations of frequency: Emboli occurred in one-fourth of the total number of cases. Out of 84 cases of embolus, the kidneys were found 57 times affected, the spleen 39 times, the brain 15 times, the liver and alimentary canal 5 times each, and the skin 14 times. The verrucose affection in its subacute form is so seldom found alone in the heart, and so generally accompanied by pericarditis, that several observers will only speak of endoperi- carditis for this reason. The combination with myocarditis is by no means so frequent. The further changes, such as fibrous thickening, cartilagination, calcification, which the valvular tis- sue and outgrowths undergo during a prolonged course of the disease, fall under the head of chronic endocarditis. Etiology. The etiology of the subacute form is in part similar to that of the diphtheritic. Rheumatic arthritis here too takes ; SUBACUTE VERRUCOSE ENDOCARDITIS. 85 the first place, and indeed it combines with the vegetative infinitely oftener than with the ulcerative endocarditis. The uncertainty of the diagnosis, in many cases, explains the great discrepancies between the estimates made by different authors as to the frequency of the combination. Great differences prevail, even on the subject of the cardiac complications in rheumatism ; and here the easier course is to make • no distinction between endo- and pericarditis. Bouillaud assumes a percentage of 55, Budd of 48, Fuller of 23, and Wunderlich and Lebert of 23. When we consider our present subject, subacute endocarditis, the variance is still greater. Bamberger finds it in 20 per cent., Lebert in 17.1, Wunderlich in 15.7, and Roth in 12.6. Accord- ing to Bouillaud, on the other hand, in every ten cases of rheumatic fever, there were eight complicated with endocarditis ; and Vernay finds even this estimate too low, especially for childhood. From this it may be seen how unfruitful these statistics are at present, and how much they depend on the expansive power of the statistician's conscience as regards diag- nosticating the presence of endocarditis. Of one thing we may rest assured, namely, that it is far oftener assumed than really present. The assumption that the severer cases of rheumatism, in which many joints are simultaneously involved, are oftener complicated than the lighter cases, is also not quite safe, though founded on more careful statistics undertaken by Fuller. I am much more inclined to side with Vogel and others, who do not recognize any such distinction between severe and light cases as regards their influence on cardiac complications. Nor can I share the opinion of distinguished physicians for diseases of children (West, Rilliet, Barthez, etc.), who assert that childhood best illustrates the connection between rheumatism and endo- carditis, because the majority of cases of rheumatism occurring in childhood is complicated by endocarditis. For I have re- peatedly seen cases of acute rheumatic arthritis, even in children, which were not followed by endocarditis ; and indeed I con- sider the disposition to endocardial affections, on the whole, smaller in childhood than after puberty. The maximum fre- quency of valvular diseases falls between the ages of 20 and 40, or 60 and 70. It is a striking fact, but one which I have 86 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. frequently confirmed, that those acute articular affections ac- quired in the course of gonorrhoea, and which are embraced under the title of " Rheumatismus gonorrhoicus," are seldom or never complicated with endocarditis, while pericarditis has been comparatively often observed in this connection. However, it is not exclusively articular rheumatism which lends a favorable site for the production of this heart disease. Thus it may be preceded in children, for example, by the caput obstipum, and in adults by muscular rheumatism. Though in by far the majority of cases the rheumatism, whether articular or mus- cular, has been first observed, and afterwards the development of the heart disease, yet there are a few well-attested cases on record where the process first localized itself in the endocar- dium, and the articular affections followed later (Graves, Stokes, Trousseau, Monneret, Gubler, Jaccoud). Childbirth and pregnancy, in general, also stand in close relations to the development of this form of endocarditis, although the connecting link between these two conditions is no more visible than in the case of rheumatism. Ollivier has, however, compiled a series of observations, which render the existence of the connection most highly probable. This period of a woman's life is rendered peculiarly dangerous, if, before her pregnancy, she has acquired heart disease. In fact, what Vir- chow calls the recurring form of endocarditis verrucosa, is far more commonly developed during pregnancy than the primary form. Old valvular diseases are in general one of the commonest causes of the subacute endocarditis. We must, consequently, distinguish between an original and a recurrent form. And in this section we have the original chiefly in view. Acute exanthematous diseases in childhood are rather pro- ductive sources of endocarditis, especially scarlatina and measles, and the former more frequently than the latter. One might easily be led to think that those rheumatoid affections, which are often observed, especially after the fading of the scar- latina eruption, were the agents to produce the heart disease, and that we have merely a repetition of the rheumatic combina- tion. However, this connection can not be proved, and the SUBACUTE VERRUCOSE ENDOCARDITIS. 87 occurrence of these rheumatoid affections is no necessary link, for the heart disease may be quite early developed, even before the exanthema has faded. During an epidemic of scarlatina I saw one child in a family attacked by diphtheritis, and the other by subacute endocarditis. Both complications produced fatal results. Although endocarditis has been observed in the course of variola, still we are scarcely authorized to speak of any connec- tion between the two. In the severe epidemic which visited Holland during my professional activity there, amongst a large number of small-pox patients I did not once see this complica- tion arise. According to Labadie-Lagrave's assertions, croup and diph- theritis are also complicated by vegetative endocarditis, and the same author even expresses an opinion (for which I can find no ground in his own observations), that in this very endocardial complication lies a cause, though one which has as yet received little attention, for the fatal issue of those diseases. Endocarditis has been observed to follow in a few cases of typhoid, but myocarditis succeeds far more frequently. Chronic or acute inflammation of the kidneys is indeed not very often the cause of endocardial disease, but still there are cases on record. But where an acute nephritis occurred simul- taneously with endocarditis, as often happens, I could only regard both as the results of a third force common to both ; but I have never observed a renal inflammation as an etiological factor in the heart disease, for they were developed quite simulta- neously. Symptoms. In many cases the disease exhibits so few general phe- nomena that anybody who is not in the habit of making a local examination of the organs every day during acute affec- tions is certain to frequently overlook the cardiac complica- tions. The general state of the system which exists previously to the endocardial disease is usually not materially altered by its advent; and the fever connected with the original ma- 88 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. lady is not necessarily altered, either in intensity or type. Only when convalescence has already begun in the articular affection, and the fever is on the decrease, then renewed fre- quency of the pulse and rise of temperature attract attention to the heart, and the patient may sometimes complain of palpi- tations. But other complaints, such as those of pain, are never made, except in cases where pericarditis or pleuritis are simul- taneously developed. The palpitations, however, annoy the patient, sometimes in a continuous form, at other times in fits, and they are accompanied by a suggestive feeling of shortness of breath. The pulse quickens and the temperature rises, though neither with any great intensity. The fever belongs to the inter- mittent type. The general condition of the patient, without any further striking symptoms, speaks for fever. In the local ex- amination of the heart we find an extended cardiac impulse; percussion proves no changes from the normal conditions in the first stages, and in auscultating we hear murmurs, when one or more valves are affected. In the great majority of cases we can only hear a systolic murmur (with or without the first cardiac sound) in its maximum intensity over the apex, corresponding to the localization of the process on the mitralis. But even in those cases where the aortic valves are the only part affected, and when, too, these valves have been rendered insufficient, the systolic still drowns the diastolic murmur to such a degree that the latter is actually altogether inaudible. Duchek's assertion that even when the disease was localized on the mitral valve, he has always heard a diastolic murmur, is strikingly at variance with the experience of most observers. Quite in the beginning of the disease, too, the second sound in the pulmonary artery is intensified. The verrucose products in themselves give rise to no physical symptoms, but the swelling and thickening of the valves, in connection with this production, are generally con- siderable enough to injure their vibratory powers, and conse- quently the most frequent sign is that we hear a systolic murmur along with the proper cardiac sound. A murmur, however, is generally heard in company with other physical signs, as when extensive growths on the edges of the flaps are so considerable as to prevent any further exact closure, or when the tips or flaps SUBACUTE VERRUCOSE ENDOCARDITIS. 89 of the valves become adherent, whether with one another or with the surface of the ventricles, or finally when thrombotic forma- tions on the valvular excrescences narrow the ostium—in a word, when an acute valvular disease is developed. Also, under these conditions the duration of the process is too short to allow of any striking expression of the secondary symptoms. But the murmur is systolic or diastolic, or both, according as insuffi- cience or stenosis preponderates, and is distincter over the apex or base, according as the disease is localized in the mitral or aortic valves. And we may easily perceive that the second pul- monary artery sound is intensified, and that the cardiac volume is transversely hypertrophied, when the disease is localized in the mitral. As regards embolism, since we have already dis- cussed its nature in diphtheritic endocarditis, and shall further describe it in connection with the chronic form, where it occurs chiefly in acute recrudescences, we need only mention here that in the verrucose form the infarction does not occur in so many organs at once; but, on the other hand, it is recognized more easily on account of the greater space it takes up in each separate organ. Clots in the spleen are in this case, as in the former one, recognized by the swelling and painfulness of the organ. Infarction often indeed produces no outward symp- toms when it takes place in the kidneys ; but when the clots are larger than usual, sudden pain is felt in the loins, and haematuria results, accompanied by albuminuria, that continues for some time afterwards ; but these symptoms do not last long. Emboli in the basilar vessels of the brain, especially in the artery of the Sylvian fissure, are proclaimed by acute hemiplegia, with or without loss of consciousness. Obstructions in the intestinal vessels, which occur occasionally, exhibit themselves in severe abdominal pains like colic, accompanied by the passing of blood. Of the peripheral arteries, those of the lower extremity are the most usually affected, and with the possible result of mortifica- tion of the toes or even of a whole limb. All embolical processes may frequently betray themselves in shivering fits, followed by perspiration. 90 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Diagnosis. There are few diseases the presence of which is diagnos- ticated so arbitrarily as that of original acute and subacute endocarditis. Bouillaud and his followers regarded every systolic murmur that occurred in the course of acute rheumatic arthritis as a symptom of endocarditis, while Vernay goes so far as to assert that he never found even the murmur a necessary support in establishing his diagnosis; increased rapidity of pulse, fever, and palpitations, are quite sufficient for him if these symptoms are rapidly developed during the course of acute rheumatic arthritis in patients who before this were healthy. We may grant that the sudden occurrence of such symptoms may be connected with some irritation of the endocardium ; but still it must be remembered that verrucose vegetations in them- selves produce no symptom at all, and can only be detected when the disturbances have advanced so far as to produce an acute valvular disease. Thus, the presence of verrucose endo- carditis can only be assumed with perfect certainty either when the physical signs display to our view the development of a valvular disease, or when we hear a systolic murmur alone on the heart in the course of rheumatic fever (or any other of the above-mentioned etiological diseases), and when this is accom- panied by visible embolical obstructions in the vessels, which cannot be attributed to any other source, such as thrombi from the walls of the ventricles. The chief difficulty here lies in dis- tinguishing mere accidental murmurs from those which indicate an actual disturbance in the function of the valve, and, further, when we have established the presence of the latter, we must prove that its origin is acute; and in this connection we must exclude all recurrent defects, such as accompany a valvular dis- ease of long standing, for the patient may not have been known before to the physician, and besides the valvular disease often runs its course without any striking symptoms. The first diffi- culty may generally be overcome by proving the existence of other symptoms in addition to the mere murmur, especially an intensified second sound in the pulmonary artery, the localiza- SUBACUTE VERRUCOSE ENDOCARDITIS. 91 tion of the murmur by ascertaining the situation of its maximum intensity, or transverse hypertrophy, even though slight, of the cardiac volume. In relation to the slighter degrees of increase in the area of actual dulness, it must be remembered that passive dilatation of the heart can take place during acute fevers, unac- companied by a valvular defect. The exclusion of the recurrent forms must be founded chiefly on the absence of any symptoms of unusual hypertrophy or dilatation of one or both ventricles ; for if these be present, and if we can exclude any obstruction in the peripheral vessels, such as sclerosis of the arteries and shrinking of the kidneys, the existence of a former valvular dis- ease may be assumed with certainty. Duration and Result. The duration of acute and subacute endocarditis is in itself relatively short, since it leads to chronic valvular diseases in most cases, and in all others terminates fatally through com- plications with affections of the cardiac substance or envelop, with myocarditis or pericarditis, or through pleuritis or pneu- monia, or finally through embolism in vital organs. I have seen it last for two or three months in cases of the latter cha- racter. Instances where the disease has been really cured are not on record, perhaps on account of timidity in diagnosticating its presence. Creditable authorities, indeed, and Fuller, in par- ticular, speak confidently of the absorption of the verrucose products and disappearance of all abnormal symptoms; but they do not give sufficient details to convince others who have not seen it. One should be especially cautious about drawing any conclusions as to the occurrence of recovery, on the ground that the murmur has temporarily disappeared. Prognosis. The prognosis is favorable in so far as life is comparatively rarely threatened by verrucose endocarditis. But, as regards a complete recovery, it is totally unfavorable, since it is almost certain to result in chronic valvular diseases. 92 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Treatment. It has been asserted that there are methods of treating acute rheumatic arthritis which prevent its complication with heart diseases. In particular the method of vesication, applying a blister near each affected joint, recommended by Herbert Da- vies, claims1 preference on this ground. Though the number of cases Davies, and others after him, have brought forward is not large enough to enable us to form a sound judgment on the success of his method, still it is a striking fact that in the majority of cases treated in this way no endocarditis oc- curred. For this reason we should most certainly further test Davies' method of treating acute rheumatic arthritis,, in its utility in warding off endocarditis, and thus at the same time meet the prophylactory indications of endocarditis, suggested by the rheumatism which is already present. When the symptoms of increased cardiac activity arouse suspicion of the develop- ment of endocardial disease, an attempt should be made to moderate the fever by the application of cold, in the shape of poultices or ice-bags. At the commencement, nitre and the tartrates of soda are suited for internal use. Though many assert that the application of blisters only excites the fever and palpitations, I cannot coincide in their opinion, and especially recommend flying blisters on the back. The fever is seldom so intense as to need special treatment; and if it do rise high, quinine, in doses of from 8 to 15 grains a day, suffices. Though it is impossible to cure any functional disturbance of the valves after it is developed, still by removing all mental and physical harmful influences, and supporting the strength of the patient by suitable diet and drugs (light animal food and iron salts), we may succeed in bringing the disease into its chronic stage, and attain the longest possible duration of an endurable state of health. Thus we must begin using tonics as soon as the fever leaves the patient. Nor must we neglect lukewarm baths, which act on the skin, and thus promote nutrition in Clinical Lectures and Reports of Lond. Hosp., 1864. CONTRACTING AND SCLEROTIC ENDOCARDITIS. 93 general, and on the whole aid the circulation. In exceptional cases, especially when large clots are formed in the heart, or when extensive infarction takes place in the lungs, disturbances in the circulation so acute and threatening may be developed in endocarditis, that intense cyanosis and dangerous oedema of the lungs require the most vigorous steps to be taken. Moderate bleeding is recommended in such cases. But as soon as the most dangerous symptoms have been banished, we must again have recourse to tonics, and sometimes even to stimulants. English physicians, after Richardson's example, lay great weight on ammonia as a solvent for fibrinous precipitates, and in Ger- many Gerhard professes to have seen favorable results from the inhalation of carbonate of soda. This latter method is worthy of further trial just in these very cases of recent endocarditis. Chronic Endocarditis and Valvular Affections. Contracting and Sclerotic Endocarditis. Besides the often quoted and universally known works of Kreyssig, Bouillaud, Hope, Walshe, Stokes, Forget, Skoda (treatise on auscultation), Bamberger, Friedreich,, Duchek, Dusch, and Fuller, the following special writings are of weight on the subject of endocarditis in general: Hasse, Anatomische Beschreibung der Krankhciten der Circulations- und Respirationsorgane. Leipzig, 1861.—Ecker, Ueber aneurysmatische Ausdehnung der Herzklappen. Heidelb. med. Annal. 1842.—Barclay, Contributions to the statistics of valvular disease of the heart. Med. Chir. Transact., 1848, and Edinb. Med. Journ. 1853.— Rapp, Zur Dia- gnostik der Klappenaffectionen des Herzens. Zeitschr. fiir ration. Med. 1849.— See, De la Choree. Mem. de l'Acad. de Med. Vol. XV. 1850; and Rapport du Rhumatisme et des maladies du cceur avec les affections nerveuses et convul- sives.—Klinger, Ueber die physikal. Untersuchungen der Krankheiten der Herzklappen. Wiirzburg, 1851.—Traube, Versuche iiber die Wirkung der Digi- talis. Berliner Charite Annalen, 1851; and Ges. Abhandlungen, Berlin, 1871.— The same, Ueber die Wirkung der Digitalis bei Herzkranken. Ges. Abhandlungen, p. 27 o.—Ruhle, Ueber Herzkrankheiten in Giinsburg's Zeitschr. III.—Beau, Considerations gengr. etc. in Archives gen. de Med. 1853.— Willigk, Sections- ergebnisse der Prager pathol-anatom. Anstalt. Prager Vierteljahrschrift, 1853 and 1856.— Virchow, Gesammelte Abhandlungen. 1856.—Traube, Ueber den Zusammenhang zwischen Herz- und Nierenkrankheiten. Berlin, 1856.— 94 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Forster, Uebersicht von 639 in den Jahren 1849-56 verrichteten Sectionen. Schmidt's Jahrb. 1858.— Buhl, Ueber Ectasien der Lungencapillaren, in Virch. Arch. 1859.— Virchow, Ueber die Natur der constitutional, syphil. Affectionen, separately printed, 1858.—Jaksch, Ueber die spontane Heilung ker Herzkrank- heiten. Prager Vierteljahrschrift, I860.— Skoda, Ueber Complication bei Klappenfehlern und deren Therapie. AUgemeine Wiener med. Zeitung, 1860. — Ogle, On ulcerations, true and false aneurisms on the valves of the heart. Transact, of Pathol. Soc. of London, 1861.—Gerhard, Zur Casuistik der Herz- krankheiten. Wiirzb. med Zeitschr. 1861.— Peacock, On some of the causes and effects of valvular disease of the heart. London, 1865.—Rosenstein, Zur Be- ziehung zwischen Herz- und Nierenkrankheiten. Berliner klin. Woch- enschr. 1865.— L. Martineau, Des Endocardites. Concours, etc. Paris, 1866.— R-lvct, Des Aneurysmes du comr. Paris, 1867—Rindfleisch, Lehrb. der path. Gewebelehre, 1867-69.—Fr. Fuchs, Ueber die mechanischen Bedingungen der Hypertrophie und Dilatation des Herzens. Dissert, Bonn, 1867.—P. Gutt- mann, Ueber die Ursachen der Kurzathmigkeit bei Herzfehlern, etc. Berliner. klin. Wochenschr. 1867.—Oppolzer's Vorlesungen liber Herzkrankheiten, von Stoffella, 1868.— Bucquoi, Lecons cliniques sur les maladies du cceur. Paris, 1869.—Rene Blache, Essai sur les maladies du cceur chez les enfants. These, Paris, 1869.—Lender, Zur Behandlung chronischer Herzkranker. Berliner. klin. Wochenschr. 1870.—Foster, Digitalis and heart disease. Brit, and Foreign Med. Chir. Review, 1870.—Fothergill, On palpitation and on cardiac irregularity. Med. Times, August and December, 1870.—Salter, On the hemor- rhages of heart disease. Lancet, 1870.— Cohnheim, Untersuchungen iiber die embolischen Processe. Berlin, 1872.— H Jaster, Ueber Aneurysmenbildung der Herzklappen. Dissert. Berlin, 1873.—Fothergill, Strain in its relations to the cirulatory organs. Brit. Med. Jour. 1873.—Handfield Jones, Cases of heart disease affording evidence respecting the action of digitalis. Med. Times, 1873.—Ponfick, Ueber embolische Aneurysmen, etc. Virch. Arch. Bd. 58. 1873.—Orth, Zur Kentniss der braunen Induration der Lunge. Virch. Archiv. Bd. 58.—Penzoldt, Ueber den hamorrhagischen Infarkt der Lunge bei Herz- kranken. Deutsch. Arch. Bd. XII.—Fothergill, The mutual relations of the heart and respiratory organs. Med. Times, 1874.—Michel Peter, Lecons de clinique med. Tom I. Paris, 1874.—Ernst Frommolt, Ueber das gleichzeitige Vorkommcn von Herzklappenfehlern und Lungenschwindsucht. Archiv der Heilkunde, 1875. The chronic form of inflammation may be localized on any part of the endocardium, and as a matter of fact has been found more frequently than the acute or subacute form on the lining of the ventricles, especially in the region of the apex close under the aortic ostium ; but still this chronic form in the majority of cases, at least in extra-uterine life, selects, like the others, the CONTRACTING AND SCLEROTIC ENDOCARDITIS. 95 valvular apparatus for its favorite seat. It occurs with the same relative frequency on the different valves as in the suba- cute form. But the chronic endocarditis on the semilunar valves is peculiar, from the fact that, at least in advanced life, it is generally connected with atheroma, being in fact a continua- tion of this. But the essential difference amounts to nothing, since both processes are perfectly analogous, and the chronic endocarditic products resemble those of endarteritis, except in the quality of contraction possessed by the former, and which plays a very important part in destroying the symmetry of the valves in chronic inflammation. The anatomical and histological changes are induced by hyperplasia of the connective tissue, which in the chronic form produces a tough, firm, and fibrous tissue. This tissue is either produced by the metamorphosis of an originally highly cellular, mucous and jelly-like tissue, or it occurs as such from the beginning. Thus, indeed, the whole disease is, in general terms, either the mere continuation of a process which began acutely or subacutely, or one which has been stealthily evolved, escaping from the very beginning the notice of both patient and physician. The production of the tough connective tissue is confined sometimes more to the borders of the valves, other times more to their insertions, but may often spread over the whole valve, and always has a strong tendency to shrinking. In proportion to the duration of the process the border retracts and shrinks more, the valve becomes stiff and its motion impeded. Its outward appearance varies according as the sclerotic tissue, as such, persists or undergoes further meta- morphoses. In the former case it may remain even for some length of time of a whitish yellow, as bright as a tendon, of the consistency of cartilage1, but otherwise smooth, though perhaps fringed on its shrunken border with one or more rows of very delicate, incrusted outgrowths. When the deeper layers of the newly-formed tissue undergo fatty degeneration, an atheromatous pap is produced inside them, which gradually presses through into the upper layers, and leaves the free surface of the valve as a superficial or deep ulcer, covered with fibrinous deposits, or impregnated with lime salts. Outgrowths of all kinds, from uiievennesses to bulbs, and often calcified, surround the edges 96 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. like stalactites. Thus in many cases fatty degeneration and calcification go hand in hand, while in others calcification is the only metamorphosis, and sometimes even advances to ossification. Simultaneously may occur adhesions, both of tip and flap of the valve with one another, and with the wall of the ventricle. The chordae tendinae are almost always involved in the process, and, since their structure is exactly similar to that of the endocardium, they undergo the same thickening, fatty degeneration or calcifi- cation. And from these tendons the process often spreads to the interstitial tissue of the papillary muscles. Whichever of these processes we have described predominates, whether shrinking, or fatty degeneration, or calcification, the invariable result is the destruction of the functional powers of the valves, or the con- striction of the ostium, to which the valve belongs. When the shrunken and contracted valvular borders cannot approach so as to touch one another, or when the shrunken condition of the chordae tendinae will not allow the points of the valves to rise to their proper level while the papillary muscles contract, then the communication is no longer completely shut off between the ventricle and auricle during systole, or between artery and ven- tricle during diastole—in a word, the valves are then insufficient. When the points or the flaps in their insertions are too stiff to lie up against the wall of the ventricle or artery (according as it happens to be systole or diastole), or when they have narrowed the space by adhesions to one another, the opening, through which the blood must pass, can no longer open to its nor- mal extent, and the ostium is constricted. Insufficience and stenosis are the constant result of chronic endocarditis, and in fact generally occur together. Indeed, when endocarditis or endarteritis is the cause, insufficience and stenosis perhaps never occur the one without the other. Still the possibility of a sten- osis, unaccompanied by any trace of valvular insufficiency, can- not be doubted ; while insufficience quite frequently occurs by itself, not only from the breaking off of a valve from its papillary muscle, but also from other causes. Besides, though valvular endocarditis is undoubtedly the most frequent, yet it is not the only cause of disturbance in the cardiac functions. Insufficience of the auriculo-ventricular valves, in particular, may be brought CONTRACTING AND SCLEROTIC ENDOCARDITIS. 97 about by other processes, especially by myocarditic changes in the papillary muscles ; this may occur quite apart from the sup- purative form, when these papillary muscles by fatty or fibrous degeneration have lost the contractile force necessary for tension of the valves. The stenosis may also arise from myocarditis, or from a swollen conus arteriosus. In the first cases, where the en- docarditic changes have not passed the first stage, it is not very easy to find post-mortem anatomical proofs of insufficience hav- ing existed ; for the thickenings and contractions in endocarditis do not necessarily of themselves prevent the valves closing. The points and flaps are so large in proportion to the diameters of the ostia, that a slight shrinking generally produces no insuffi- ciency, and even a more extensive degree can be compensated by expansion of the unaffected part of the valve. It will conse- quently not be out of place to mention here that the method of pouring in water, commonly used to test how far the valves can close, only gives approximate results ; for the difference between the pressure of a small quantity of water and the work done by the ventricles in raising the column of blood, is so enormous, that we can draw no comparison between them as to their effect on the valves. Thus by this method we often maybe led into diag- nosticating insufficiency of the aortic valves, and perfect closure of the mitral, when neither the one nor the other has existed during life. Aside from clinical phenomena, purely anatomical proofs in doubtful cases should be based more on changes in vol- ume or weight of the whole heart or distinct divisions of it, than on the state of the valves themselves. A post-mortem examina- tion can lead to no conclusion on any temporary insufficiencies which may have been produced, for instance, by imperfect con- traction of the papillary muscles. It is also very difficult to form a sound judgment in cases of "relative insufficience,'''1 where the only anatomical abnormality we can find is that the valve is unable to completely close the opening, owing to the un- usual state of dilatation of this latter. Friedreich has proposed a very suitable method for measuring the proportion between the surface of the valve and the circumference of the orifice in such cases. .He cuts out the orifice and measures its length; then, assuming the ostium to be a circle, he calculates its diame- VOL. VI.—7 98 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. ter by means of the formula, R= ^—. The measurements of the absolute heights of the valves are then compared with this diameter. Thus, as we see from the nature of the anatomical causes of insufficience and stenosis, the two nearly always appear in com- pany, and insufficience only occurs without stenosis in those rare cases where it arises from the loss of a valve or its adhesion with the surface of the ventricle. The possibility of an unmixed stenosis must be acknowledged in those severest of all cases, where there is no space left for regurgitation of blood ; but such cases are of the utmost rarity. On the contrary, the case of com- monest occurrence is where the two are together, but either the one or the other so preponderates, and, both from anatomical and clinical points of view, throws the weaker so into the shade that, on the principle a potior i fit nominatio, we are only entitled to speak of one of the two in our diagnosis. Causes and Frequency of the Valvular Defects. The etiology of valvular defects can only be determined directly in the one case of subacute endocarditis origin. Very frequently the'development is throughout of a chronic nature, and the actual beginning is so concealed from, and inaccessible to, both the perception of the patient and the observation of the physician, that it is almost or quite impossible to determine the influences which may possibly have acted on its develop- ment. We can only make one very general statement, namely, that these defects of the auriculo-ventricular valves are so far different from those of the aortic valves, that the former, if their origin be subacute, may often be referred to the same etiology which was described for subacute endocarditis, i. e., to rheumatic arthritis, pregnancy, and acute exanthematous dis- eases. Aortic valvular diseases, on the other hand, are incom- parably oftener developed in an insidious way, and are so fre- quently met in the most intimate connection with changes in the walls of the vessels, that one is more inclined to refer their origin to those forces which we know, from experience, to cause CONTRACTING AND SCLEROTIC ENDOCARDITIS. 99 atheroma, namely, to age, alcoholism, gout, and, what has lately been rendered more than probable, chronic nicotine intoxication. The investigations made by Ricord, Lebert, and Virchow have demonstrated beyond all doubt that syphilis also is one of the causes of endocarditis ; but as the changes here are more confined to the parietal part of the endocardium than to the valves, and can scarcely be separated from simultaneously occurring changes in the muscles, they can be better treated under the head of myo- carditis. Corvisart's assertion, that syphilitic excrescences, especially condylomata, occur on the valvular endocardium, has met no confirmation from subsequent observers. However, there are isolated cases of syphilitic valvular endocarditis on record, the most noteworthy being one communicated by Leared,1 where the aortic valves were attacked. In harmony with the influences at work, we find that mitral affections occur more in youth, and aortic more frequently in advanced years. Still this statement must be accepted with considerable reserve. Workmann 2 has observed aortic insufficiency even in a child of four years old, and I myself have an exquisitel}r marked case in a boy of ten, while stenosis of the aortic ostium from endocarditis has been seen repeatedly (see Blachez). In regard especially to affections of the aortic valves, it remains to point generally to the influence mechanical and traumatic (especially a rupture of a valve flap by falling) causes may have, and also to mention strain due to over- exertion—a matter which has received especial attention lately in its etiological importance from Albutt, Myers, and Seitz. The frequency of valvular defects is of course in direct pro- portion to the frequency of those circumstances which are etio- logically connected with it. But one thing we must remember, namely, that there is by no means any adequate proportion between the occurrence of valvular disease and multiple rheumatic arthritis. For instance, in Holland I am bound to assert that acute multiple articular rheumatism is a relatively seldom occur- ring form of disease, while valvular disease is just the opposite. This agrees with Hirsch's testimony to the fact that the geograph- ical distribution of heart diseases is represented by no area, dis- 1 Transac. of Pathol Soc., London, 1868. 2 Ibidem. 100 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. tinguished from others by any geographical or climatological peculiarities, and characterized by the frequency or rarity of these diseases in comparison with the numbers in other, differ- ently situated, regions. Still the discrepancies which exist be- tween the statistics of various observers are astoundingly large; Duchek, for instance, estimates their frequency at 2.4 per cent., while Chambers calculates it at 17 per cent. The reason of this lies partly in the sources which have served for compiling the sta- tistics. Duchek made his estimate from the number of patients who came into hospital, and Chambers from the number of cases he found in the dead-house. However, even taking the statistics of mortality as our standard, Chambers' estimate is far too high. Let us take a larger number of cases ; for instance, the total number of post-mortem examinations in the Prague and Wiirz- burg pathological institutions amounts to 7,347, and only 677 of them were cases of valvular disease, making a total per- centage of eight or nine. Amongst the 7,870 post-mortem ex- aminations Frommolt made in the city hospital, he only found 277 cases of valvular disease, and thus a percentage of 3.5. In this connection it is scarcely necessary to remark on the arbi- trariness of statistics based only upon the post-mortem examina- tion, since the limits of anatomical changes due to chronic endocarditis are extremely elastic. Although calculations made from the number of patients taken into hospital are likewise unsuited to represent the propor- tional frequency of a disease, yet they come nearer to the truth, incomparably nearer. The books of my public dispensary record during nine years a percentage still lower than that given by Duchek, so that I am inclined to regard one or two per cent, as the approximate proportion. No definite influence of sex is strikingly perceptible. Still it seems to me, from the literature of the subject, and from my per- sonal experience, that women, especially in their early years, suffer more frequently than men from valvular disease. The Effects of Valvular Defects in General. Whenever a valvular defect exists, on whatever valve it may CONTRACTING AND SCLEROTIC ENDOCARDITIS. 101 be, and whether it consists of insufficience or stenosis, it always produces a mechanical effect on the relations of the circulation in general, and thus brings about secondary anatomical changes, both in the heart itself and in distant organs. The mechanical effect produced by all valvular defects is a diminution of the quantity of blood which reaches the aorta, or (as it is termed when all its branches are included) the aortic system, with each ventricular systole. This effect is most directly and strikingly exhibited in those diseases which result in stenosis of the left ostium venosum or aorticum. In the first case less blood flows into the ventricle during diastole, and in the second less blood is driven out- of the ventricle during systole; but the same takes place when the mitral is insuf- ficient, for then a certain quantity of blood flows back with every systole into the auricle, instead of into the aorta. When the aortic valves are insufficient, since the left ventricle is supplied from two quarters with blood, a larger quantity than the normal is pumped into the aorta by each systole, even if the impelling force remain unchanged ; notwithstanding this, the aortic system is not so well filled as normally, for the blood which is pumped in does not remain, but regurgitates in great part. Deficiencies in the tricus- pid and the valves of the pulmonary artery produce quite as pal- pable results, though less directly; for both lessen the supply of blood to the pulmonary veins, and thus diminish the quantity which reaches the left ventricle, and consequently the quantity, too, which this ventricle can impel into the aorta. As Traube has very thoroughly demonstrated, the normal medium tension of the aortic system, provided its elasticity is unimpaired, depends on its receiving the normal supply of blood, and this again depends on the equilibrium between inflow and outflow. Conse- quently any force which lowers the inflow, and thereby also the supply received by the arteries, must directly reduce the ten- sion in the aortic system. The immediate result of a fall in the tension of the aortic system is retardation of the whole circula- tion ; for the circulation is dependent essentially upon the differ- ence of pressure in the arterial and venous systems in so far as everything which raises the pressure in the aortic system, cceteris paribus, hastens the circulation. In the given case, of valvular 102 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. defects, this difference is not only diminished by the lowering of the arterial tension, but the scale is actually turned in favor of the venous system. For the quantity of blood which the aortic system has lost collects at first indeed in the heart, dilating its chambers, beginning with that which lies immediately before the obstruction to the outflow, or the one which receives an abnormal supply. But when the chambers of the heart have been filled out to a certain extent, then the veins are overfilled, for, owing to their slight elasticity and great powers of expansion, they have a greater capacity than the arteries. And, since the tension rises in pro- portion as they are more filled, the tension of the whole venous system is raised, but still never so as to counterbalance the fall in that of the arterial system, as the elasticity and capacity of the two are so disproportionate. Every valvular disease would have to exhibit the same mechanical effect as we have just described, and every patient display symptoms of such a disturbance in the circulation, if the force of the heart remained exactly w7iat it was at the begin- ning. But this latter factor in reality does not remain the same in the majority of cases. We find, on the contrary, that those sections of the heart which lie before the obstruction to the out- flow, or those which are subjected to the pressure of an over- supply, are not only dilated, but also hypertrophied. The size of the muscle has increased in direct proportion to the dilatation, or, in other words, the additional resistance is met by additional power, represented by the propelling force of the ventricle. The effect of this additional increase of work depends essentially on the proportion the muscle bears to the capacity, and the hyper- trophy to the dilatation. We can easily imagine a balance be- tween the two so perfect as to quite compensate any disturbance in the circulation. Thus the dilated left ventricle may become hypertrophied to such a degree that its increased power enables it to drive all the blood, which has collected in it during the diastole, into the aorta at every systole; and in this way the diminished filling of the aortic system, which would otherwise necessarily result from insufficiency of the aortic valves, is coun- teracted. In many cases these secondary changes in the heart actually do accomplish this compensation, and for a long time CONTRACTING AND SCLEROTIC ENDOCARDITIS. 103 hinder the occurrence of serious circulatory disturbance. But of course it very rarely happens that the balance is quite per- fect. For, even when the compensatory work falls to the left ventricle—chiefly, we may say, in defects of the aortic valves— the correction is only just sufficient for the most ordinary con- ditions ; and in remedying these defects, the action is more pre- cise than in any other case. But even here the respiration is always impeded the moment the smallest extra demands (such as active exercise, walking up a hill, etc.) are made on its exer- tions. This is still more marked in defects of the auriculo- ventricular orifices, and cases where the compensation is so accu- rate as to obscure all symptoms of disease, are of the extremest rarity. For ordinary circumstances, however, the correction may be quite sufficient to allow a patient with heart disease to attend to his business for years, provided the business is not of a strenuous nature. But it is quite plain that these relations may assume very various forms. For instance, if the general nutrition of the patient be deficient, no compensatory hypertro- phy at all need take place; or, a very common case, the cardiac muscle is hypertrophied, but not in proportion to the extent of dilatation ; or, finally, compensation takes place, but is destroyed, either by organic diseases, which throw new obstacles in the way of the circulation, and thus make fresh demands on the activity of the heart (bronchitis, pneumonia, pleuritic exudation), or by direct disease of the heart itself and its envelopes (degen- eration, whether fatty or of connective-tissue nature, and pericar- ditis). In each of these cases there exists a disparity between the resistance and the power ; and the effects we originally described, as produced on the circulation, namely, diminished tension in the aortic system, and a higher tension in the venous, with a retarded circulation, all these may be recognized both by ana- tomical and functional disturbances. The disturbances in com- pensation are earlier and more markedly apparent in the respira- tory apparatus, in those valvular diseases in which the powerful compensatory force, which the left ventricle can supply, is want- ing, or is only furnished in an insufficient manner. The influence which this retardation of the stream produces may be perceived in the heart as clots, found sometimes in the valves, and some- 104 ROSENSTEIN.—DISEASES OF TnE ENDOCARDIUM. times on the walls ; on the latter they collect between the meshes of the trabeculae carneae, and more especially in the auricles. We have already shown how much harm these clots may do, when fragments of them, as emboli, block the circulation in the vessels of remote organs. Without entering minutely into the details of how infarctions are formed—a task which Cohnheim has already performed in such a masterly manner—we must once more call attention to the fact that it has been demonstrated that the presence of " terminal arteries" and " valveless veins" (in the spleen, kidneys, brain and eye) is a prerequisite for the reversal of the blood-current in the veins, this being the first result of the engorgement of the district in question; it is only after the reversal of the current has taken place that the walls of the vessels undergo functional changes that lead to hemor- rhage—the characteristic feature of infarctions. Thus the clots, which so often occur in chronic endocarditis on the walls of the right ventricle and the auricles, attain a great importance as the genetic origin of the hemorrhagic pulmonary infarction, a secondary condition of great weight in valvular diseases. Here we find hemorrhagic knots, and centres of induration, which occur sometimes alone, at other times in groups; are most fre- quently situated in the periphery, seldomer in the centre; generally in the inferior lobes of the right lung, and not so often in the left; they are cuneiform, of a dark blue or reddish- brown hue ; their base points to the pleura, and their apex to the hilus of the lung. Though these are favored by the increased side-pressure in the pulmonary arteries, still there is not the slightest doubt but that they are in great part, though not always (as there are well-established cases, too, of infarction due to stagnation), produced by embolic obstruction of the smaller branches of the pulmonary artery. Cohnheim has shown that in the peripheral portions of the lung the branches of the pul- monary artery, from the manner in which they form anasto- moses, are, in a functional sense, terminal arteries, and thus fulfil the conditions which, as he has proved experimentally, are necessary to produce hemorrhage, after closure of an afferent branch. However, from the fact that we find this far oftener in diseases of the mitral than in those of the aortic valve, it is CONTRACTING AND SCLEROTIC ENDOCARDITIS. 105 evident that increase of pressure in the pulmonary is not alto- gether without its influence on the production of pulmonary infarction. The symptoms by which pulmonary infarction may be rec- ognized during life are the sudden appearance of dyspnoea (often accompanied by a shivering fit), and along with it a pain- ful cough ; this is soon followed by a mucous expectoration tinged with blood, or even by more or less haemoptysis. If the infarction is peripherally situated and not confined to an extremely small area (or if several large infarctions are coin- cidently present), it may be detected by physical signs of induration of the tissue, i. e., dulness of the percussion sound and bronchial breathing. Gueneau de Mussy2 professes to have perceived a peculiar smell in the breath, in these cases, of a garlic character, and which he supposed to be the result of changes in the blood that came into direct contact with the atmosphere; but I have never succeeded in detecting it. The infarction is seldom accompanied by fever, never in my own experience. Even in cases where, in addition to a number of in- farctions, there was engorgement of the entire lower lobe, I have failed to discover fever ; on the contrary, the temperature was as low as from 9S.2° to 98.8° Fahr. Still other observers (Gerhardt and Penzoldt) assert that they have seen the temperature rise. This would produce such an exact likeness to pneumonic infil- tration as to render it extremely difficult to distinguish one condition from the other. And this difficulty is greatly in- creased when, as frequently happens with infarction of the periphery, the case is complicated by pleuritis. The hemor- rhagic infarction may heal, and afterwards we can find no post- mortem traces of it beyond a scar. Thus it frequently runs a harmless course, but it is equally certain that it may lead very rapidly to death by gangrenous decomposition. This occurs, for example, when the infarction becomes infected by the embolus. It is this element of infection that the patient has most to fear in an infarction, and not its localized effects. In other cases, again, a fatal termination follows speedily after the occurrence 1 Gaz. des hopitaux, 1871, No. 34. 106 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. of infarction; but here death does not take place as an im- mediate result of the infarction, but rather on account of its occurrence toward the end of life, when the heart's action is constantly growing feebler. All other changes, however, which we find in the respiratory tract of patients suffering from heart disease, must be ascribed to stagnation. At the commencement the only important sign of disturbance beginning in the compensation is congestion, which may be diagnosticated by a dry cough. When the stagnation advances, we seldom fail to find the rales, and mucous or muco- purulent sputa, characteristic of bronchial catarrh. In fact, this bronchitis is often the very first symptom of disturbance in the compensation, and for this reason deserves most particular at- tention. When the stagnation is very great, as happens espe- cially in stenosis of the left ostium venosum, haemoptysis, unaccompanied by infarction, is by no means a symptom of rare occurrence. The parenchyma of the lungs, too, undergoes some- what extensive changes. Then naturally the nutritive functions are disturbed in the walls of the vessels, which are under a con- tinuous high pressure. Dittrich has called attention to the fatty degeneration of the intima coat of the smaller branches of the pulmonary artery. Of equal importance is the dilatation of the capillaries which, as Virchow and Buhl have demonstrated, can reach such a height that they become varicose, and their shoots project far into the lumen of the alveoli. In this way the space is curtailed and dyspnoea is produced by a purely mechanical cause. When this condition is accompanied by slight hemor- rhage into the alveoli and the interstitial tissue, the interlobular tissue undergoes hyperplasia, and at the same time we have that peculiar change in the lungs termed red-brown induration. The whole substance of the lungs is reddish-yellow, colored by the transformation of the coloring matter of the blood into granular pigment; besides this, they are generally large, tough, and heavy, but disproportionately emphysematous. In a case which Orth observed, in addition to the pigment deposits in the cells of the alveoli and connective tissue, he found in many places numerous capillaries and even larger vessels with a diameter of from 0,063 to 0,075 mm., filled up with the same pigment as that CONTRACTING AND SCLEROTIC ENDOCARDITIS. 107 in the interstitial connective tissue. The formation of pigment in the alveoli is the cause why pigment-filled cells are coughed up with the sputa. When we see them, we may infer the presence of this abnormal condition of the lungs even during life. The cells are characterized by the smallness and plainness of their nuclei; their origin is not quite certain, still Rind- fleisch's supposition, that they are wandering cells from the blood, seems to me rather far-fetched ; it is much more probable that they are derived from the pulmonary epithelium. When the insufficiency of the heart is so great, that the blood in the over-filled pulmonary vessels stagnates continuously, oedema of the lungs sets in, and this, in the tissue full of pigment, imparts here also a tinge to the sputum, which earns it the name of brown cedema. In all these anatomical changes in the lungs we can find quite sufficient grounds for the production of short- ness of breath, of which the patient most frequently complains, sometimes before any other symptom, even in the conditions of compensation, could lead to the detection of the disease. How- ever, it is clear, that when the ordinary conditions of circulation do not prevail, we do not at all need any coarse anatomical lesion to explain the dyspnoea, while, on the other hand, addi- tional causes, of more exceptional occurrence, may take part in producing it. The overfilling of the capillaries with blood, and the accompanying retardation in the circulation, are of themselves quite sufficient to disturb the exchange of gases in the lungs ; and the result of this being an insufficient oxidation of the blood, would cause a subjective feeling of want of breath. Besides the circulation in this case loses the assistance, which (as Diesterweg has so cleverly demonstrated) it receives from the respiration under normal circumstances ; for the respiratory movements act not only as suction, but also as pressure pumps, on the circulation ; but in this case the capillaries cannot stretch any more during inspiration. Though all these factors play a prominent part, yet the purely mechanical causes claim a large share of importance. We have already noticed how ectasia of the capillaries may narrow the lumen of the alveoli. In other cases the left lung is compressed by the hypertrophy of the left ventricle. This can reach such a height, that I have occasion- 108 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. ally, in making a post-mortem, found the whole anterior border of the left lung quite concealed by the hypertrophied heart. In extremely rare instances the primary bronchus has been known to be compressed by dilatation of the left auricle ; cases of this kind are recorded by King and Friedreich ; the latter has even diagnosticated it during life. With this constant shortness of breath arising from the above-mentioned causes, we must not confound sudden fits of dyspnoea. These are especially frequent in connection with dis- ease of the aortic valves, and are characterized by intense want of air (Lufthunger), though the respiratory movements are un- affected. This dyspnoea is often accompanied by pain, felt in the cardiac region, spreading to the arms (especially the left arm), and arousing a suspicion of angina pectoris. There has not as yet been enough physiological or anatomical proof brought for- ward to allow the assumption that these fits are connected with irritation of the plexus cardiacus, which lies behind and beneath the arch of the aorta. The foundation is laid in the respiratory disturbances for the more important changes in the blood, at least for those of the exchange of gases, which are so clearly expressed in the com- plexion of patients suffering from heart disease. This is the cause especially of the cyanosis, which, when the circulation is disturbed, becomes visible on all those parts which even under normal conditions exhibit a bright coloring ; as the lips, ears, and tongue. The blood-corpuscles, on account of the long time they remain in the capillaries, while the blood flows so slowly through the peripheral vessels, lose far more of their oxygen and take up a more abundant supply of carbonic acid; and again as they pass through the lungs they take up less oxygen than usual, and get rid of less carbonic acid. Both these processes tend to de- stroy the bright scarlet color of the blood, and produce a darker, blue-red tinge. It is of course only in congenital defects of the pulmonary artery (especially its contraction), where we have the greatest mechanical disturbance in the exchange of gases, that the most intense cyanosis occurs; and in this case the whole body is more or less of a dark-blue color, more particularly the peripheral parts, the extremities. Still, cyanosis is never com- CONTRACTING AND SCLEROTIC ENDOCARDITIS. 109 pletely absent even in the mildest cases of disturbed circulation ; the practised eye will often detect the treacherous blue flush in what to all appearance is the fresh, red hue of the lips. The cyanosis always becomes more intense when extra demands, such as physical exertion, are made on the exchange of gases. When the stagnation has advanced so far as to produce a cya- notic color in the skin, it can be further recognized in the over- filled condition of the peripheral veins. The small veins of the face, which were before scarcely visible, now project in meshes ; and in the neck we can see both the internal and external jugular veins so plainly, that their respiratory movements are nearly always quite perceptible, and sometimes even pulsatory move- ments. This over-filling generally begins in those vessels in which the circulation has to raise the column of blood, and thus under normal conditions is inclined to go slowly. Consequently, in the lower extremities it is not confined to the mere projection of blue cords, but the vessels, owing to the constant strain, be- come varicose and contorted, and their fibrous coat grows thick. When coagulation commences in these vessels, painful oedema of the affected parts results ; and the process may extend from the branch far into the trunk. We have seen how the clots on the walls and valves of the heart may be carried off by the circula- tion, and become wedged into the main trunks, the branches of which supply the lower extremities ; and how they here become the causes of necrosis and of moist or dry gangrene, that begins in the toes and spreads upwards. In the same way the particles from thrombi in the lower extremities get into the right side of the heart, and give rise to pulmonary infarction, which we have already described; and where they obstruct the trunk or larger branches, they assume a great importance for the whole process, since they may produce sudden death. The more the peripheral veins are filled, the greater is their tension, and, in consequence, the pressure which the walls exert on their contents is increased. And this intensifies the transudation of serum from the smaller veins and capillaries, which takes place under normal conditions. At the same time resorption is rendered more difficult, and the lymph can only be emptied with greater labor, so that there is reason enough for the collection of serum in the meshes of the 110 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. subcutaneous tissue. In heart diseases, oedema always com- mences in the lower extremities ; at first it is scarcely noticeable, then it is perceived in the evening about the malleoli and on the dorsal aspect of the feet; but after a night's rest in the horizon- tal position, it cannot be any more seen in the morning. As the disease advances, the dropsy spreads upwards, first up the lower extremities, then over the sexual apparatus ; finally it comes to the superior parts, and, in the very worst cases, it appears even on the face. Of the internal cavities, the peritoneal is the first to suffer from transudation, for local causes are here at work in the affection of the region of the portal vein. Next to this come the pleural cavities, especially the left one, and with it generally the pericardium. The dropsy is not a mere symptom of disease, but it constitutes a new ring in the chain, which literally hems in a patient with heart disease. The pressure which the transuded fluid exerts on the smallest vessels creates new resist- ance to the circulation, and makes fresh demands on the activity of the ventricles. The skin is disposed to inflammation from being soaked with serum, and when the oedema is very extensive the epidermis is raised in blisters. These burst, and then follows an erysipelatous inflammation of the surrounding skin; and when an inactive diuresis leaves the blood rich in urinary com- ponents, deep-seated phlegmonic inflammation in the subcuta- neous cellular-tissue gives rise to tedious suppuration, which is generally the commencement of the final stage. Though the hindrance to the circulation is the chief, yet it is not the only cause which produces dropsy. The change in the oedema alone, whilst the mechanical conditions remain unaltered, and the various areas it covers in the same original disease, point to other causes. Thus it is not improbable that a considerable part in the production of the oedema may be played by disturbances in the vascular innervation, and together with this by the changing conditions as regards the participation of the whole propulsive force which proceeds from the vessels. One factor, which comes into account here, is well determined—namely, the loss of albumen and solid components which the blood under- goes. The changes in the blood are as little confined to the darker CONTRACTING AND SCLEROTIC ENDOCARDITIS. Ill color of the corpuscles and their supply of oxygen as the effects of stagnation are confined to the respiratory organs. The digestion, too, the chief factor in producing and sustain- ing the solid components of the blood, suffers as the disease advances. When the stagnation spreads to the hepatic veins, the circulation in the liver and in the whole drainage region of the portal vein—the stomach, intestines, and spleen—is retarded, and this gives rise to important anatomical and functional dis- turbance. At first the liver is swollen and h}Tpertrophied by the abnormal quantity of blood it contains, and especially the left lobe ; this enlargement is f"It by the patient as a sensation of ful- ness and pressure in the hepatic region and epigastrium, and may be diagnosticated by palpation and percussion. Corresponding to this is the post-mortem appearance of the organ ; when exam- ined in the first stages of the disease, it is large, heavy, contain- ing a very large quantity of blood, and the central lobular veins extremely full. But the cellular elements of the central parts soon undergo atrophy, and when the peripheral parts contain enlarged cells filled with fat, they become clearly marked off from the more central atrophied and bluish-red colored portions, and thus, as a whole, exhibit the well-known appearance of the nutmeg liver. As the process goes on, the peripheral parts atrophy as well, and this, together with compression and hyper- plasia of the interlobular connective tissue, which results from long-continued venous hyperaemia, render the liver tough and indurated. When actual inflammatory processes take place in the connective-tissue, they may lead to a real cirrhosis ; but still we may have objective symptoms of atrojiihy without cirrhosis. Since perihepatic irritations often accompany the disease, the patients complain of pain in the region of the liver, both of a spontaneous nature, and also on pressure. The formation of gall is always affected in these cases, as may be seen, too, in the alteration of its composition ; but real intense icterus only occurs when the outflow of gall is hindered by a catarrh of the mucous membrane of the ductus choledochus. A light jaundice tinge, especially when mixed with slight cyanosis, may be seen on the conjunctiva and face, when the liver begins to be involved in the disturbances, and the pressure of the dilated veins on the gall 112 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. canals retards the progress of the secretion, without altogether stopping it. Of the organs which belong to the territory of the vena portse, the stomach and alimentary canal are always involved, while the changes in the spleen are not so constant, and, moreover, cannot be recognized by any functional disturbances, since swelling, hyperaemia, and unusual toughness are the only anatomical symptoms of splenial disease. On the other hand, the symptoms in the stomach and alimentary canal are most strongly marked: the appetite is lost, and a feeling of satiety follows quickly on eating, while constipation and diarrhoea succeed one another— in a word, the whole digestive system is disordered. In the cases in which vomiting of blood, or passing of it with the stool, are recorded, the hemorrhage was perfectly independent of the ordinary stagnation, being caused by embolism in the arteria coro- naria ventriculi and the mesenteric arteries. There are, as yet, very few cases of this kind on record (Virchow, Bekman, Cohen, Oppolzer, Gerhard, Kussmaul); they generally exhibited severe intestinal hemorrhage, which came on very suddenly, accom- panied by sharp pains like colic in the abdomen, and a consid- erable fall in the temperature ; in some cases peritonitis, with or without vomiting, set in. The digestive derangement is a very important factor in the sum of the disease, and exerts a great influence on the course, since it interferes very materially in the formation of blood, and thus adds to the mechanically impeded circulation the further complication of cachexia. The functional disturbances in the kidneys are an exact reflection of the alterations of the vascular tension. And here we can observe, better than on any other organ, the various stages of decrease of the quantity of blood in the aortic system, and in- crease of that in the venous system; for the varying conditions of the urinary secretion enable us to see both the serial succes- sion and the development of these circulatory derangements. If, in any unit of time, a smaller quantity of blood flows through the glomeruli, the quantity of the secretion diminishes like- wise ; according to Ludwig and GoU's experiments, the quantity of water is more affected than that of the solid components. Accordingly the volume of urine passed in twenty-four hours CONTRACTING AND SCLEROTIC ENDOCARDITIS. 113 decreases, when the tension in the aortic system falls in valvular disease, and the solid components are relatively increased—in other words, this urine has a high specific gravity. "When the urine cools, the salts of the saturated solution are soon precipi- tated, and on the bottom of the vessel we see a deposit, consist- ing chiefly of urates, and rich in urinary coloring matter. If the patient is well fed, we may often see crystals of pure uric acid in the sediment; they are generally cylindrical, and occur in great numbers. The urine becomes albuminous as the ten- sion increases in the venous system, just as H. Meyer and others found when they ligatured the vena cava above the junction of the renal veins. The interval at which albuminuria succeeds the first-mentioned process varies greatly for different cases. Symp- toms of venous stagnation may present themselves in other organs long before they can be seen in the kidneys. The quan- tity of albumen varies with the degree of tension. It is gener- ally accompanied by the appearance of jelly-like sacs in the urine, in the shape of liyaline cylinders. But blood-corpus- cles are exceedingly seldom to be found in any number in the urine from a stagnant circulation ; and haematuria never occurs unless there be simultaneous inflammation of the interstitial tissue. This inflammation does sometimes occur, although nephritis is entirely unconnected with the paradigm of stag- nation in the kidneys. If the kidneys are examined at the commencement of the disease, they will be found enlarged, hyperaomio, and of a tough consistency. In a later stage they are atrophied, tough, and have a cyanotic appearance. The cortical substance appears thickened in section, at first striped with red, and further on of a grayish-yellow color. The cortex and medulla are distinctly bounded; the basilar part of the medullary substance is of a darkish color, while the part turned to the papillae is quite pale. Under the microscope the glomeruli appear of normal size, the convolutions are generally intact, the capsule slightly thickened and more separated into layers than normally. In the tubules the epithelium is very granular, quite frequently fatty, and sometimes filled with fine pigment. The membra na propria of the uriniferous tubes is thickened, the inter- stitial tissue is thickened, and very fibrous. The great majority VOL. VI.-8 114 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. of cases answer to the description we have just given, so that Traube and those who adopt his view are right in asserting that this passive hyperaemia in the kidneys is a disease, sui generis, which cannot be put in the same category with the initial stages of inflammatory derangement of the nutritive process in these organs, or diffuse nephritis. But, besides this, there are a few cases in which advanced anatomical alterations are found in the kidneys, simultaneously with valvular disease of the heart; these are usually regarded as the product of interstitial nephritis, whether it be diffuse fatty degeneration or atrophy. It is only by clinical observation of their development that we can decide what relation exists between the cardiac and renal diseases. We know that, as a matter of fact, valvular heart disease follows in the course of chronic nephritis, and this has already been dis- cussed in the section on subacute endocarditis. But in reality this occurs relatively seldom. On the other hand, I have repeatedly convinced myself, that, from the very beginning, the development of the cardiac and renal diseases ran parallel, which leads me to regard the two as co-effects of a third, and genetically independent of one another. However, there are frequently hemorrhagic infarctions in the kidneys of patients suffering from heart disease, which occur in the shape of wedges, with their base looking towards the cortex, and their apex towards the hilus, being caused by obstruction in the branches of the renal artery; and we must not forget that these too give rise to interstitial inflammation. Consequently, in our consider- ation of the connection between valvular disease of the heart and inflammatory anatomical changes in the kidneys, we must not forget to reckon infarction as etiological. Many assert that the renal pelvis and the bladder participate in this stagnation, but I have never seen a case of pyelitis or catarrh of the bladder which was due exclusively to valvular defect in the heart. On the other hand, the effects of an obstructed circulation are much more visible in the sexual organs, at least in the female organs ; for irregularities in menstruation occur extremely often in females who have valvular heart disease. Amenorrhoea com- mences before cachexia assumes a very pronounced form ; but in the earlier stages the menstruation is generally very profuse, CONTRACTING AND SCLEROTIC ENDOCARDITIS. 115 and occurs at abnormally short intervals. The shape which the derangement takes is essentially dependent on whether general anaemia is more prominent, or whether the obstruction to the venous outflow preponderates. The form taken by the symptoms of a deranged circulation in the nervous system, and more especially in the brain, varies with the seat of the valvular defect and its nature. Patients with a stenosis of the aortic orifice very soon exhibit signs of arterial anaemia in the shape of frequent fainting-fits, which occur while all the other functions seem undisturbed and with- out any apparent cause, and moreover pass away quickly when the horizontal position is assumed. When the auriculo-ventricu- lar valves are affected, the most prominent symptoms are those of venous hyperaemia. The patients complain of headache, dizziness, and a whirring sound in the head; and females, in particular, very often have the feeling of clavus hystericus. Cor- responding to these complaints, we sometimes find in the post- mortem examination dull patches in the meninges, and some- times extensive oedema in the sub-arachnoid, with slight effusion into the ventricles ; but these affections probably do not originate during lifetime. Obstructions may be seen in the cerebral vessels, both in the small twigs of the cortex and in the larger branches at the base. Death is often the immediate result of a simultaneous obstruction in several cerebral arteries. Murchison ' describes a very marked case of a girl, 14 years old, whose mitral valve was affected, and the particles of a fresh fibrinous clot obstructed both the vertebral and the internal carotid at the same time. The symptoms of hemiplegia appear suddenly when the arteries of the Sylvian fissure are obstructed, and this is often followed by softening of the cerebral substance. An embolus so frequently makes its way into the left artery of this Sylvian fis- sure, that right-sided hemiplegia has been regarded as a means for diagnosticating embolic paralysis. However, in diagnosticating a central paralysis inpatients with heart disease, from the fact that the patient has a valmilar disease, or from the attack fall- ing on the right side, we are not entitled to assume with absolute 1 Transact, of Path. Society of London, 1871. 116 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. certainty that the paralysis originated embolically. Others, as well as myself, have repeatedly observed ordinary apoplectic spots in similar cases, without any obstruction in the afferent vessels. Nor must we forget that, to produce an embolus, the affection of the valve must be acute and recent; and hence, as a result of chronic valvular disease, we must look for it in company with the recurrent form. As a general rule, we m&y assert that of all valvular diseases those of the aortic valves are the ones most usually accompanied by fatty degeneration of the small cerebral vessels and consequent hemorrhage in the brain. Thrombi and apoplexies, especially the latter, are frequently the cause of death in cases of insufficience of the aortic valves, and they must be taken into account in making the prognosis of a valvular affection, which is otherwise so often well compensated. Saccular aneurisms, which Ponfick has lately found on the vessels of the base of the brain, may be mentioned, besides fatty degeneration, as anatomical causes for sudden death and the disturbances generally proceeding from the brain. The special characteristic of these aneurisms was a wall chiefly composed of a thin layer of connective tissue and thrombotic deposits of various thickness, while a spinous, chalky embolus lay free in the aneurismal cavity, or projected into it with its point. This form of aneu- rism is most usually found in cases of endocarditis of the aortic valves. As regards their genesis, it is very important to note that the emboli always stop a short distance from the bifurcation of a vessel, and being here sharply pressed against the wall of the artery by the greatly increased pressure of the blood which flows into the side branch that remains pervious, they probably destroy these walls by " decubital necrosis:' Doubt has been thrown on the assumption Nasse made, as to the great frequency with which pronounced psychical derange- ment, actual " mental diseases," resulted from cardiac disease. The statistics of the post-mortem examinations made in lunatic asylums go against him, for, according to Griesinger's calcula- tions, only 12.5 per cent., out of 602 autopsies made in the Vienna Lunatic Asylum, exhibited valvular disease ; and, even in these, the connection between the two affections had not been clinically established for all. Griesinger himself, too, does not consider CONTRACTING AND SCLEROTIC ENDOCARDITIS. 117 mental disease a frequent result of cardiac affections. Still, it cannot be denied that light psychical alterations are peculiar to patients with heart disease, and are often reflected in their features ; these are expressed in the shape of oppressed, melan- choly temper, feeling of dread, and abnormal excitability. In a case of insufficiency of the mitral which came under my observa- tion, I saw flts of actual confusion and strange behavior, while in the intervals the patient was extremely apathetic and unsym- pathizing. Of course, such isolated cases do not suffice to prove a genetic connection, but if we consider that in the post-mortem examination we sometimes can demonstrate the presence of thromboses in the vessels of the cortex, and join the two facts together, we obtain what may form a material foundation for psychical disturbance, and a causal nexus is rendered probable, certainly for the cases quoted. The functions of the spinal cord are never disturbed by valvular disease, unless (as some do) we regard St. Vitus' dance, which so often occurs, espe- cially in childhood, along with chronic endocarditis, as a dis- ease of the spinal cord. In fact, the anatomical centre of origin of chorea has not yet been established for certain, and, as far as the investigations hitherto made on the sub- ject go, they point more to the brain than to the spinal cord as the probable seat of the disease; some facts speak for the English observers, Broadbent, Hughlings Jackson, Tuckwell, and others, who assert that it is a capillary embolic affection of the corpus striatum. What, however, chiefly interests us here is the fact, which was first brought forward by See, Roger, and other French physicians, that chorea minor is frequently found combined with valvular diseases of the heart and acute rheumatic arthritis. The proportions which Roger assumes are certainly too high, for he asserts that out of 71 cases of chorea, 47 were combined with simple endocarditis, and 19 with peri-endocar- ditis ; the only way to account for his assertion is that he diag- nosticated endocarditis on the insufficient ground of a systolic murmur over the heart. Considering the anaemic condition of most chorea patients, these murmurs, of course, prove nothing. However, Ogle, too, found fibrinous deposits on the valvular endocardium in 10 out of 16 cases of chorea which ended fatally. 118 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. The connection with multiple rheumatic arthritis is not so pro- nounced; for instance, out of 252 cases of this latter, Steiner only observed 4 cases of chorea. My own observations confirm the frequency with which mitral affections are complicated by chorea, especially in very young patients. On the other hand, I have seen two cases of rheumatic arthritis, in which the chorea was developed before the valvular disease. What we have said will give an idea of the principal changes produced in the different organs by a derangement of the circula- tion, which results from valvular disease. We must now describe the symptoms afforded by a physical examination, these being immediately dependent on changes in the valves. But these symptoms can be best treated in connection with the individual peculiarities which are produced by the diseases of the different valves, and figure even in the general sketch. So we shall pass on to the consideration of the diseases of the different valves. Affections of the Left Auriculo-ventricular Valve and the Left Ostium Venosum. In addition to all the handbooks, consult: Briquet, Memoire sur la diagnose du retrgcissement ventriculo-auriculaire gauche. Archives ggnSrales de Med , 1834.—Herard, Des signes stethoscopiques du retrecissement de l'orifice auri- culo-ventriculaire gauche du cceur; ibid. 1853 and 1854.—Duroziez, Du rhythme pathognomonique du retrecissement mitral. Arch. gen£r. 1862.— Traube, Eine Bemerkung uber das Verhaltniss der tuberculosen Pneumonic zu organischen Herzkrankheiten. Berl. med. Centralzeitung, 1864.—Leyden, Ein bemerkens- werther Fall von Stenose des Ostium venosum. Virch. Arch. 1864.—Nauvyn, Ueber den Grund, warum hin und wieder bei Mitralinsufficienz das Systol- gerausch am lautesten in der Gegend der Pulmonalklappen zu horen ist. Berl. klin. Wochenschrift, 1868.— Geigel, Der gespaltene Herzton. Wurzburger Ver- handlungen, 1868.—Guttmann, Ueber den gespaltenen diastolischen Herzton. Virch. Arch. 1869. — Quincke, Ueber accidentelle Gerausche in der Pulmonal- arterie. Berl. klin. Woch. 1870.—Bucquoi, Lecons cliniques, etc. Paris, 1870. —von Bamberger, Ueber zwei seltene Herzaffectionen, etc. Wiener Wochen- schrift, 1872.—Koster, Braune Induration mit crouposer Entziindung der Lunge. Virch. Arch. 1873.—Balfour, Clinical lectures on diseases of the hpart. Edinb. Med. Journal, 1871.—J. Wickham Legg, Mitral constriction, and well- marked concentric hypertrophy of the left side of the heart Transact, of Pathol. Society of London, 1874. INSUFFICIENCY OF THE MITRAL VALVE. 119 Insufficiency of the Mitral Valve. Of all the different causes which produce insufficiency of the mitral, by far the rarest are the acute, such as the breaking off of a valve (whether from its basilar insertion or from the papillary muscle by rupture of the chordae tendinae) or perforation from ulceration, or finally the development of an aneurism on the valve. In the majority of cases it is produced by the subacute and chronic forms of endocarditis, quite as frequently by the fibrous thickening and contraction of the valve itself as by the shortening of the chordae tendinae and their adhesion to one another. The verrucose vegetations, if present in large quanti- ties, may also injure the closing power of the borders of the valve, but in their ordinary extent they never produce this effect. Adhesion of the point of the valve to the ventricular wall brings about the purest form of unmixed insufficience. The same may occur in the course of fever, where it has been occasionally observed, being due to derangement in the innervation of the papillary muscles. It may occur, too, where these muscles are rendered incapable of developing the force necessary to hold back the valve, having lost their contractility from fatty or fibrous degeneration. But in the great majority of cases the insufficience is complicated with more or less stenosis, and so we can only prop- erly speak of the preponderance of the one or the other affection. In a certain sense, we can regard a slight stenosis as compensating the insufficience, since the mechanical operation of the latter is to some extent weakened by the former. The insufficient valve no longer shuts off the left auricle from its ventricle during the sys- tole, and consequently the blood is driven simultaneously into the aorta and the left auricle. The aorta receives proportionately less blood, while the auricle is over-filled, being now supplied from the left ventricle, in addition to its ordinary supply from the pulmonary veins, and is thus subjected to a higher tension. The larger quantity of blood, which reaches the left auricle, dilates it, and the symptoms of increased tension are easily recog- nized in the hypertrophy of its walls and the opacity of its endo- cardium. This rise in tension is propagated from the left auricle into the pulmonary veins, and if these too be examined, traces 120 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. are found of nutritive derangements in the form of hypertrophied walls, fatty degeneration, and here and there jelly-like prolifera- tions on the intima. The increased tension next extends through the capillaries of the pulmonary artery into the right ventricle, right auricle, and finally into the whole venous system. The general reversal of pressure, the diminished tension in the aortic, and increased tension in the venous system, common to all val- vular defects, is so arranged in insufficience of the mitral valve, that the tension is highest in the pulmonary veins and venae cava-, and lowest in the aorta. All parts of the heart which lie before the mitral orifice are thus dilated, and are hypertrophied in direct proportion to their normal muscularity. So, for in- stance, the right ventricle is much more hypertrophied than the left auricle, this latter being more dilated. But the left ventricle, too, is generally hypertrophied, the reason being that it is filled during the diastole under the high pressure which prevails in the pulmonary veins, and must consequently perform its function under a higher pressure. During the whole course of these successive changes in the substance of the heart, the patients hardly experience any an- noyance. They are, indeed, very little troubled, till the compen- sation is deranged by some pathological process in the cardiac muscle (especially fatty degeneration of the right ventricle), by diffuse bronchitis, or by disease of the pericardium. The patient perceives the vain efforts which the diseased muscle makes to empty its abnormally large contents, in the form of palpitations. These often occur without any special outward cause, but gener- ally commence when larger demands are made on the circulatory organs, as, for instance, during active exercise. Along with this, the patient has a feeling of shortness of breath, since even quick respiration cannot supply the increased demand for oxygen. And, complaining of this annoyance, he generally has recourse for the first time to medical aid. It may happen that the phy- sician some time before has witnessed the subacute commence- ment of the valvular disease in a febrile attack of rheumatic arthritis; but, even in this case, years may elapse before the patient thinks it necessary to again put himself under treat- ment. It is frequently the dry cough, produced by congestion INSUFFICIENCY OF THE MITRAL VALVE. 121 of the bronchial vessels, which brings the patients to consult a doctor. Objective examination then shows, that the cardiac region projects abnormally, and is more arched. This is espe- cially prominent in youthful cases. The cardiac impulse is seen and felt lower down than usual, generally between the sixth and seventh ribs, and either in the mammillary line, or more frequently 2 or 3 cm. external to this. The impulse is more extended, espe- cially to the right, and undulatory movements are visible even in the epigastrium. The resistance of the impulse is increased, and a purring sensation may often be felt in its neighborhood, syn- chronously with the ventricular systole. Percussion shows that the boundaries of the areas of absolute and relative dulness are extended both to the right and to the left. The area of dulness generally extends as far as the impulse to the left, but often goes even a little beyond this. The outlines of the area of dulness are seldom irregular ; they generally form a triangle, in such a way that the left limb runs abnormally to the left in its lower end, but above it remains within the mammillary line. On the infe- rior portion of the sternum the sound is dulled, but the border of the right lung is seldom so far displaced as to produce further dulness to the right of the sternum. The inferior part of the right limb of the triangle of dulness coincides with the right border of the sternum, or lies at most 2 or 3 cm. outside it. We cannot lay too much stress on the importance of testing how far the an- terior border of the lung moves, and of excluding all other causes for dulness, before diagnosticating an increase in the volume of the heart from an increase in the area of dulness. In auscul- tating close under the nipple, and a little to the left, we can hear a systolic blowing murmur, which either completely takes the place of the first cardiac sound, and continues to the short pause, or is heard along with, and then only at the commencement of, the first sound. We can often detect the presence of the sound along with the murmur, by raising the ear slightly from the disc of the stethoscope. Though this murmur is propagated over the situa- tions of all the other orifices, still it is very easy to perceive that the greatest intensity is over the apex. Very often we hear the murmur on the left border of the sternum in the second intercos- tal space, /. e., in the situation of the ostium of the pulmonary 122 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. artery, quite as loud as over the apex, and sometimes even more intensely. This cannot be explained by the approach of the pulmonary artery to the thorax wall, brought about by displace- ment of the left lung, for we can easily convince ourselves by percussion that the vessel is covered by the lung. Nor can it lie in the greater tension of the walls of the pulmonary artery, for though a murmur might be thus produced, yet it is not evident why it should be more intense in this situation ; and besides, as far as the pulmonary artery is concerned, the same conditions prevail in stenosis of the left ostium venosum, but still the mur- mur cannot be heard so plainly. The greatest probability attaches to Naunyn's explanation. He points out that the given situation of maximum intensity in the second left intercostal space does not correspond exactly to the place where the sounds of the pulmonary artery are heard—that is to say, not quite at the edge of the sternum, but about 2" from it. From investiga- tions made on the dead subject, it appears that this point would coincide with the point of the left auricular appendix which winds round the pulmonary artery and lies in front of it. Since the abnormal current of blood, which in insufficience of the mitral valve gives rise to the murmur, flows towards the auricle, and since the auricular appendix communicates freely with this, we can easily comprehend how the sound should be conducted to the spot mentioned better than towards the apex, and be heard there with greater intensity, more especially in strongly-marked cases where the appendix is long enough to lay its point close against the anterior wall of the thorax. Beside the systolic murmur, we may hear a diastolic (or pre- systolic, as the case may be) murmur; but this depends on whether the ostium venosum is simultaneously constricted, and on the degree of stenosis. In most cases, the second sound cannot be heard quite pure at the apex. But as the pulmonary artery is under greater tension, over it the second sound is heard more intensely than normal, while the right ventricle continues to exert more force in the performance of its functions. It is not till the force of the right ventricle has been injured by disease of its muscle, that we lose this important symptom of an intensified second sound in the pulmonary artery. The diagnostic signifi- INSUFFICIENCY OF THE MITRAL VALVE. 123 cance of this symptom was first pointed out by Skoda. So long as the compensation continues to suffice, the peripheral vessels are quite normally supplied, and the pulse does not necessarily ex- hibit any abnormalities either in rhythm or in frequency, although at this stage it is generally rather rapid. But as soon as the compensation is disturbed, and the symptoms of stagnation be- come plain, both on the visible vessels and in the internal organs, then the pulse, too, begins to lose its normal character. It grows rapid, low, soft, unequal, and irregular. The sphygmographic tracing in this affection has nothing characteristic about it. In Marey's work (loc. cit. p. 525) one can observe this great diver- sity of pulse, for scarce one tracing is exactly similar to another. When Marey remarked, " Le pouls dans l'insuffisance mitrale est toujours irregulier," he probably had the stage of deranged compensation in his mind. Fig. 9, for instance, is a tracing taken in the stage of compensation, and all we see in it is, that it is very low, and strongly dichrotous, but it is almost quite regular. Fig. 10 shows that relative regularity may co- exist with waves so exceedingly small as to be scarce traceable. Fia. 9. ^JWW^VJWW^ Fig. 10. The course of the disease is such, that the symptoms of stag- nation assume a permanent character, and all the more so in pro- portion to the greater number present. Though at first it is generally possible to reduce the palpitations and dyspnoea by suitable diet and drugs, and temporarily even to remove all oedema, yet, after a long period of alternate relatively good health and total incapacity for motion or work, the patient be- comes gradually anasarcous, and exudations begin to fill up the serous cavities and impede the respiration. Bronchitis, of which 124 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. more or less is always present, increases the cyanosis, and, whether it be accompanied or not by a pneumonic induration, often developed towards the end of the disease, the usual termi- nation is oedema of the lungs. In a few isolated cases the actual, though distant, cause of death is embolic obstruction in the cerebral vessels and its usual results, or extensive apoplexy. Embolism of the pulmonary vessels does not occur so frequently as in stenosis of the mitral orifice, but, on the whole, it is not rare. Shivering fits, dyspnoea, and bloody sputa are the first symptoms. If the infarction be somewhat extensive, there will be percussional dulness, and bronchial respiration may be heard. I have never seen a single case where fever occurred. Gerhard and Penzold have, however, observed this. Towards the close of the disease we often see thrombosis of the peripheral veins, generally confined to the lower extremities, and one-sided. Clots in one or more large arteries of the lower extremities are fortu- nately of rare occurrence. These may result, when they do occur, in mortification of the toes, the foot, or even of the whole leg, as in one case which came under my observation. The diagnosis must be based solely upon the physical symp- toms we have mentioned, and is in the majority of cases unat- tended with difficulties. However, the fact that similar physical signs may be produced by other conditions, may sometimes ren- der it quite hard to discover the real state of the case. Hyper- trophy of the right ventricle and a louder second sound in the pulmonary artery, may result from any marked derangement in the lesser circulation, quite as often as from an affection of the mitral valve. Besides this, a systolic blowing sound may frequently be heard in cases of emphysema. In cases of this kind the only means of preventing the confusion of the two is, to make a careful examination into the development of the whole disease, and to ascertain if the patient has previously suffered from rheumatic arthritis, whether he has had a cough for a long time, or whether there be any emphysema, etc. It is easy to dis- pose of those cases of chlorosis, too, which lead us to falsely as- sume a disease of the mitral valve, on the ground of any temporary dilatation of the heart, in addition to the murmur that is heard over the apex. And besides, in cases of this nature, the second STENOSIS OF THE LEFT OSTIUM VENOSUM. 125 sound in the pulmonary artery is seldom louder than usual, the murmur over the apex partakes more of the character of an organic murmur, and may usually be heard over the base as well, and the general state of the constitution points unmistakably to the real primary disease. Lastly, there is a class of cases, which, though not of frequent occurrence, still most certainly do some- times occur. These are spontaneous dilatations of the heart, quite independent of any anatomical change in the valves ; they are very misleading, for the relative insufficience of the valves that accompanies them produces a murmur, and at the same time we observe all the symptoms of cardiac hypertrophy. In instances of this kind, it is absolutely impossible to distinguish this from an insufficiency caused by anatomical changes. Seitz' s excellent observations, made in Biermer's Clinique, have proved this in the most instructive manner. The prognosis in this valvular disease, though certainly un- favorable as regards total recovery, is still relatively favorable. For the compensatory action, produced here both by the right and by the left ventricles, may often suffice for a long period. There are cases on record of patients who have lived over fifteen years with a valvular disease. Any intervening diseases, how- ever, whether cardiac, pericardiac, or pulmonary, alter the prog- nosis very much for the worse. Young patients bear the affec- tion better than old people; the danger is very great during pregnancy, and, in cases of women attacked in this state, the issue is often suddenly fatal. Stenosis of the Ostium Venosum Sinistrum. Whilst insufficiency of the mitral valve may in some cases, according to its anatomical nature, occur quite by itself, stenosis of the orifice occurs almost unexceptionally accompanied by insufficience of the valve. For the stiffened and hypertrophied valve, which is no longer able to lie flat against the wall of the ventricle during ventricular diastole, has not only a border in greater part shrunken (and thereby alone incapable of closure), but is so altered, too, in its flexibility, that the ten- sion of the papillary tendons no longer suffices to bring the 126 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. borders into perfect contact. It is only in the most extreme cases of stenosis, such as those that are brought about by a cohesion between the borders of the valvular flaps, which only leaves a narrow split for the passage of the blood from the auricle into the ventricle, that the contraction of the papil- lary muscles is still capable of closing the small space. Even in the rare instances where the stenosis has originated acutely in large fibrinous deposits on flaps, or in a coagulation pro- jecting into the orifice from the auricle, there generally is some trace of insufficience of the mitral valve present at the same time. However, the physical signs of stenosis are so prominent in the clinical view of the symptoms, that we are entitled to discuss this as the predominant derangement. The mechanical action of this stenosis is to hinder the blood, brought from the pulmonary veins into the left auricle, in its passage into the ventricle. The left ventricle consequently receives an abnormally small supply of blood, and must thus propel less into the aorta during the systole. So we see the very same results produced as in insufficience of the valve, only that the stagnation in the pulmonary vessels and venae cavae is more intense, since the left ventricle here is not filled under abnor- mal pressure, as in the former case, and the powerful lever of compensation, formed by the hypertrophy of the left ventricle, never comes into play. The anatomical changes found in the several parts of the heart in the post-mortem examination quite correspond to these relations. The left auricle is dilated and hypertrophied, and in its appendix we frequently find a throm- bus ; the walls of the pulmonary veins are thickened and dis- colored, and covered with white spots ; the capillaries of the pulmonary artery are in a state of ectasis, and in some places varicose; the right side of the heart is dilated and hypertro- phied ;—the left ventricle, on the contrary, is smaller and atrophied. It appears, in fact, so insignificant beside the right ventricle that it might be mistaken for a mere appendage of this one, which now alone enters into the formation of the cardiac apex. The aorta, too, in consequence of this diminution in the size of the left ventricle, is abnormally narrow so that its diameter above the valves may be considerably reduced. This STENOSIS OF THE LEFT OSTIUM VENOSUM. 127 condition of the left ventricle, though the rule, is still liable to exceptions, and even in cases of extreme stenosis, the left ven- tricle has been found of over normal weight and volume. Friedreich has tried to explain this fact, in the absence of any further complication, by assuming that the increased tension in the venous and capillary systems of the body can produce an additional resistance to the arterial current, great enough to counteract the tendency in the left ventricle to diminish in size. It appears fair to include as well the two other factors of simulta- neous insufficiency of the valve, and a contraction of the aortic lumen. If the nutrition be good, the latter must directly tend to hypertrophy even during its development, while the former counteracts atrophy. A physical examination during life gives the following results : In some cases the apical impulse is visible within the mammillary line, between the fifth and sixth or the sixth and seventh ribs. But in the majority of cases extensive undulations are visible, which pass beyond the normal limits, both to the right and to the left. Owing to the horizontal position assumed by a very much hypertrophied right ventricle, the systolic motion may be seen to extend to the anterior axillary line towards the left, and beyond the right border of the sternum to the right. The resistance of the apical impulse is very weak, and in bad cases it may be quite imperceptible. In palpating, the finger feels a purring vibration over the cardiac apex ; this generally precedes the cardiac systole immediately, and is consequently presystolic ; but it may be purely diastolic in many cases. Frequently one can perceive a simultaneous systolic vibration. Percussion shows an increase in both absolute and relative dulness as well to the right as to the left. The dilatation of the right auricle, when very considerable, may be recognized by a noticeable dulness to the right of the sternum. Auscultation does not always give similar results. Eddies are produced in the blood, as it flows from the wide auricle during diastole through the narrow orifice into the ventricle, and these eddies give rise to a murmur. Consequently the murmur produced by stenosis can only be heard during the diastolic phase. And, indeed, this harmonizes with a number of cases in which one only hears a 128 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. diastolic murmur, or along with this a systolic murmur as well, since there is nearly always more or less insufficience of the valve. The diastolic murmur is blowing or grating, somewhat uneven and protracted, and extends to the succeeding systole. This protraction may be easily understood, if we consider how much longer the diastole must last to permit the same quantity of blood to flow through a constricted opening as would flow through an orifice of the normal size. In many cases the mur- mur is not properly audible till towards the end of the diastole, when the simultaneous contraction of the auricle increases the force of the current, as at the beginning of the diastole the rate of the current is not great enough to produce this. Con- sequently it immediately precedes the systole, and Gendrin, who was the first to study it closely, has given it the name of presystolic. The first cardiac sound immediately follows on this, and is usually loud and intensified ; sometimes it is pure, but more generally accompanied by a murmur. The majority of cases answer to this description, but occasionally the contrac- tion of the auricles does not suffice to accelerate the current of blood to the degree necessary for the production of this mur- mur ; and thus it sometimes happens that we hear no murmur, notwithstanding the presence of stenosis. We may accordingly distinguish three sets of cases in rela- tion to the auscultatory phenomena : first, when we have a purely diastolic murmur ; secondly, a presystolic ; and thirdly, no murmur at all. The murmur proper to the stenosis always reaches its maximum intensity over the apex, or even a little to the left of this, since the current of blood takes that direction. The murmur is often more audible when the patient lies on his left side, instead of on his back ; and even when no murmur can be heard while the patient keeps in a position of rest, one can generally be perceived after active exercise, or when he is put lying on his left side. In addition to the murmur, we have| another auscultatory phenomenon peculiar to stenosis. In a few cases (by no means so frequently as Geigel assumes) we may hear over the apex, and very distinctly over the pulmonary artery, a reduplication of the second cardiac sound, which pro- duces a rhythm, called, after Bouillaud's example, the bruit de STENOSIS OF THE LEFT OSTIUM VENOSUM. 129 rappel. Geigel called attention to its frequency of occurrence in stenosis, and explains it by the unequal tension in the aorta and pulmonalis, which may prevent the synchronous closure of the valves of the two vessels, since the aorta with its smaller contents contracts quicker, and thus closes its semi-lunar valves an instant before those of the pulmonary artery. The fact that the second part of the reduplicated sound may be heard much more accentuated over the ostium of the pulmonalis, lends a great deal of probability to the view that it is produced by the valves of this artery. Even where there is no reduplication, the second sound is more intense in the pulmonary artery, when the ostium venosum sinistrum is constricted ; this is due to the greater tension of the vessel, and may be heard more plainly than in mitral valve insufficience, since in this case the second aortic sound, on account of the small tension in the aorta, is in itself weaker than normal. When the tension decreases in the pulmonary artery, the intensity of the second sound ceases ; this takes place either when the right ventricle's force has been impaired by disease in the performance of its increased work, or when the right side of the heart is so filled by the increased stagnation that the ring of insertion of the tricuspid valve is widened, and the valve is no longer able to close the orifice. Relative insufficience of the kind frequently occurs in cases of mitral stenosis, especially towards the end of life, and may be diagnosticated by the symptoms peculiar to this affection ; these we shall enter into more1 particularly when treating of this form of valvular defect. Fig. 11. Fig. 12. The condition of the pulse is more characteristic in stenosis than in insufficience of the mitral. The frequency and rhythm, VOL. VI.—9 130 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. indeed, may be normal, but the peripheral vessels are left so empty that the smallness, emptiness, and softness of the pulse serve as special landmarks. Of the two tracings we give here, the first displays a still perfectly regular pulse, with a slight systolic elevation and a scarcely perceptible elevation from recoil. The second (Fig. 12) shows the most marked irregu- larity, being taken after the compensation had been destroyed. In this case a purely diastolic murmur was heard at the apex. I cannot agree with Marey's view that the tracing of the pulse exhibits variations in regularity, according as we hear a dias- tolic, presystolic, or simultaneous systolic murmur; nor can I assent to his assertion, that, "when the mitral constriction is sufficiently marked to give rise to a diastolic murmur, it de- stroys the irregularity of the pulse" (loc. cit., p. 520). It is unnecessary to repeat here all the symptoms of stagna- tion developed with the increase of disturbance in the compensa- tion, both in the peripheral vessels and in the internal organs; they occur here in even greater degree in mitral stenosis than in insufficiency of the mitral valve. The complications in the lungs, the dark-red induration, and hemorrhagic infarction occur more frequently in cases of stenosis than where the in- sufficience preponderates. Haemoptysis often occurs without any hemorrhagic infarction. The opinion used to prevail that it would be quite unwarrantable to connect this with the initial stage of phthisis. For observers, even of such large experience as Traube, have never seen caseous pneumonia developed under such conditions, when at the same time the right ventricle was hypertrophied, so that it would appear as though this valvular defect gave immunity from phthisis. However, Frommolt's re- sults contradict this, for he found that out of all the cases in the post-mortem room of the Dresden Krankenhaus, where he met with valvular disease, that 10.8 per cent, (and amongst them dis- eases of the mitral ostium, and even stenosis of the ostium venosum sinistrum) occurred in company with pulmonary con- sumption. Thus this questionable immunity requires at least a new investigation. Icterus, without any catarrh of the gall-ducts, has been ob- served as a sign of stagnation more frequently in stenosis than INSUFFICIENCY OF THE AORTIC VALVES. 131 when insufficience predominates. In the cases which have come under my investigation acids of the gall were found in the urine. The diagnosis of this valvular disease is only difficult in cases where no murmur can be heard or where a systolic mur- mur alone is audible on account of the simultaneous insuffi- cience. Under these conditions it is impossible, and as yet of no practical importance, to avoid the confusion with simple in- sufficience. But the condition of the pulse alone will excite the suspicions of the observer as to the existence of merely this latter. In the majority of cases the presystolic, and in others the purely diastolic murmur, heard with greatest intensity over the apex of the heart, is an unerring guide, and, if we take into review the results of the percussion, renders our decision easy. The prognosis is more unfavorable in cases where stenosis predominates than where insufficience is predominant, for the compensation is rendered easier by the share which the left ventricle takes in it. Still, the compensation brought about by the right ventricle alone, as experience teaches us, may suffice to sustain life endurably for years, and exceptionally even for more than ten years. But we must not forget that such cases are of an extremely exceptional order. Diseases of the Aortic Valves and of the Ostium Arteriosum. Besides the text-books already given, consult: Corrigan, Inquiries into a new disease of the heart. Edinb. Journ. 1836.—Costa Alvarenga, Memoire sur l'insuffisance des valvules aortiques, etc. Paris, 1856, and Union Med. 1863.—Lambl, Ueber papillare Excrescenzen an den Semilunarkla23pen der Aorta. Wien. Wochen- schr. 1856.—Luschka, Ueber zottenformige Bildungen an den Semilunar- klappen der Aorta. Deutsche Klinik, 1856.—Maurice, De la mort subite dans l'insuffisance des valvules sigmoides de TAorte. These, Paris, 1860.—Duroziez, Du double souffle intermittent comme signe de l'insuffisance aortique. Arch. gener. 1861, and Gaz. hebd. 1865. and R6ponse k Mr. Traube, in Gazette heb- domadaire, 1873, No. 7.—Botkin. Medic. Klinik in demonstrat. Vortragen. Berlin, 1867.—Traube (Frdntzel), Ueber Zwei eigenthumliche Phanomene bei Insufficienz der Aortenklappen. Berl. klin. Wochenschr. 1867.—Duroziez, Des Maladies organiques du cceur et de l'Aorte et du double souffle crural de l'origine saturnine. Gaz. des Hop. 1867.—Traube {Frdntzel), Zwei Falle von 132 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Stenose des Ostium der Aorta. Berl. klin. Wochenschr. 1867.—Marey, Note sur un nouveau signe de l'insuffisance aortique. Gaz. Med. de Paris, 1868.— Beared, Aortic valve disease apparently caused by syphilis. Transact, of Path. Soc. 1868.— Gueneau de Mussy, Lecon clinique, etc. Gaz. des Hop. 1871. —0. Becker, Ueber Retinalarterienpuls bei Insufficienz der Aortenklappen. Monatschr. fiir Augenheilk. 1870.—Michel Peter, L'insuffisance aortique, etc. Union med. 1871.—Riegel, Ueber den Doppelton u. s. w. Deutsches Archiv, 1871.—Hoffmann, Der Duroziez'sche Doppelton u. s. w. Berl. klin. Wochenschr. 1872.—Robert King, Extreme aortic stenosis. Path. Trans. 1873. —Foster, Clinical lecture on rupture of the aortic valves from accident. Med. Times, 1873, December.—Michel Peter, Lecons de clinique medic. T. I. 1874. Insufficiency of the Aortic Valves. Slight anatomical changes frequently occur in the aortic valves without causing any disturbance in the mechanism of their closure. To this class belong those jelly-like thickenings, the soft-tufted proliferations of the endocardial connective tissue around the nodulus Arantii, or atrophy of the same towards the border, causing the so-called " fenestrations." Even these latter produce no derangement, as they are generally mere slits, and lie between the free border and the line of closure. But when several of these become confluent and form one large opening, they too may produce insufficience. Another cause which may produce this incapability to close, are the wart-like and polypous excrescences, if situated along the line of closure, and when they fringe the whole border of the flap, partly as chalk and partly as fat, or when this border exhibits irregular gaps and cuts between the warts, as frequently happens. On the other hand, chalky deposits in the basal parts, even when of some extent, can exist without any injurious results. But the insufficience is generally produced by fibrous thickenings of one or two (seldom of all three) flaps, accompanied by considerable contraction of the borders, and consequent diminution of the height of the flap. We may further mention as anatomical causes of rarer occur- rence: the formation of an aneurism on a flap of the valve, with or without perforation, the breaking off of a flap from its insertion and adherence of one to the wall of the aorta. Though in all the changes we have mentioned there generally occurs a INSUFFICIENCY OF THE AORTIC VALVES. 133 lateral coalescence between the two flaps, still insufficience is in most cases the only result, either because the union is not exten- sive enough to produce stenosis, or, as is usually the case, because the septum brought about by coalescence soon atrophies, and later on only exists as a small border between the two flaps united now to one. The close relation of the large flap of the mitral to the aortic valves generally entails an affection of the mitral, when endocarditis attacks the aortic valve. Still the endocarditic process may occur exclusively confined to the semi-lunar valves, and the mitral be entirely free. But, as a fact, endocarditis is by no means so frequently the origin as disease which com- mences in the walls of the aorta, for these are but seldom quite free from atheroma, of which we generally find most just above the valves, and from here it spreads downwards on to the valves. Many observers still question the possibility of a rela- tive insufficiency of the semi-lunar valves, independent of any anatomical changes in the valve, and resulting purely from too great expansion of the initial part of the aorta, and consequent over-dilatation of the orifice. I myself have never seen any con- firmatory cases, and must accordingly leave it an open question. The mechanical effect of this insufficience is a regurgitation of blood during the diastole of the ventricle, proportionate to the degree in which the valve remains open, and thus the left ven- tricle is supplied not only from the auricle, but also from the aorta. This produces dilatation of the ventricle (especially its portio aortica) so great that the longitudinal sulcus no longer corresponds to the actual line of separation of both ventricles, since the septum bulges very abnormally into the right ventricle. The ostium venosum sinistrum, too, is in consequence always dilated, and the flaps of the mitral are stretched and lengthened. The increase of force, necessary to propel the larger quantity of blood, supplied from both sides, into the aortic system, must correspond to the dilatation of the ventricle. And though in general the dilatation appears more considerable than the increase in volume, yet in most cases the hypertrophy bears a very favorable comparison with the dilatation—that is to say, it is well developed. On opening the pericardium, we see that the left ventricle occu- pies a very large space, and not only is it the sole factor forming 134 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. the apex, but this apex projects, too, lower ,han the end of the right ventricle. On further observation we see that the thickness of the wall of the left ventricle has increased more than any- thing else, and that it often measures more than from 2 to 3 cm. and even at the apex. 1 or 1$ cm. Often, indeed, the volume of the wall is not absolutely greater, but still, in comparison to the breadth of the ventricle, it looks hypertrophied. The papillary muscles are not proportionately enlarged with the other parts of the left ventricle—that is, they are not round and hypertrophied, but generally, as Traube first pointed out, lengthened and flattened, corresponding to the considerable strain to which they are exposed during diastole. It happens exceptionally that the right side of the heart is simultaneously a good deal hypertrophied, though no cause for it can be found in the lungs. And in two cases I have seen the process so far advanced, that the right ventricle actually formed the whole of the apex by itself. The physical signs exhibited by this class of patients arise chiefly from hypertrophy of the left ventricle. The cardiac im- pulse is visible outside the mammillary line, as far as or even to the left of the anterior axillary line, lower down than usual, generally between the sixth and seventh ribs, but often too between the seventh and eighth. The impulse is broad, raising sometimes an area of 3" (in breadth) with some force ; in other cases we see no defined impulse, but only a systolic elevation which raises the whole thorax. Further, we observe considerable palpitations in the jugulum, vigorous pulsation of the carotids, and in many cases too a pulsation on the right border of the sternum at the level of the second intercostal space, and corre- sponding to the position of the aorta ascendens. In palpating with the finger, we experience considerable resistance from the cardiac impulse ; over and along the sternum, especially about the third sternal cartilage on the right, we may often feel a dias- tolic vibration, which, indeed, may be also felt at the apex, though very much less plainly. The percussion shows a considerable increase in the area of dulness, both relative and absolute, espe- cially in its long diagonal. It generally begins high up, on the third and sometimes even on the second rib, extendino- to the INSUFFICIENCY OF THE AORTIC VALVES. 135 sixth or seventh rib, crossing the mammillary line as high up as the nipple, and passing downwards and outwards—sometimes two inches outwards. To the right also the boundary of dulness gen- erally passes over the right border of the sternum. Botkin records cases in which the dulness has extended a little beyond the situation of the impulse, and similar cases have occasionally come under my own notice. In case the arch of the aorta is dilated, as so often happens, we find a dulness from 1 to 2 cm. broad running from right to left in an oblique direction over the manubrium sterni. In auscultating the heart we hear a weak first sound over the apex, and a diastolic murmur, the intensity of which increases as the ear approaches the base, and becomes most distinct about the third right sternocostal articulation. The murmur is especially marked over the sternum, and particularly along the left border ; it is propagated along the course of the aorta, and is loudest in the left interscapular space. Its character is almost invariably a whirring, rushing one. In the situation where we generally auscultate the aorta, the first sound is either short and definite, or is accompanied by a murmur, which may have its origin in the simultaneous stenosis, though it more frequently arises from the passage of the blood into the enlarged aorta ascendens. In nearly every case a systolic murmur is audible on the carotid arteries, and at the same time we may feel a vibration. The gentlest pressure of the finger on the vessel intensifies the vibra- tion greatly. We may look for the origin of the systolic carotid murmur in the vibrations of the arterial walls. For, since the vessels which lie so near the heart can empty their contents during the diastole into the heart as well as into the capillaries, their tension falls very low, and then is raised very high during the next cardiac systole, through the expansion from an immense wave. And in this transition from a low to a high tension vibrations are easily produced. Though this explanation is generally received, and appears the most probable, yet after Talma's experiments the murmur may be regarded as a murmur in the blood, produced by eddying movements of the fluid par- ticles, arising from the sudden increase in pressure during the systole. The physical conditions are in reality here the same as 136 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. in Talma's order of experiment. On the other hand, I maintain that when, as in other cases, a systolic sound is heard, it can be produced only by the vibrations of the vascular walls, since, according to our present knowledge, only a murmur and no sound can be produced by these eddies. During diastole there is either no perceptible sound at all over the carotids, because no sound capable of propagation arises from the aortic valves, or else we hear a murmur propagated from the aortic ostium. Even when one part of the semi-lunar valve is still capable of vibration, the sound produced by these vibrations is concealed at the ostium itself by the murmur ; yet still it may happen that we can perceive a second sound in the carotids, though over the very ostium of the aorta nothing can be heard but a diastolic murmur. Quite as considerable changes of tension take place in the peripheral vessels during systole and diastole as in the carotids, only differing in degree ; they are also perceptible both to the ear and to the touch. In the first place, the radial pulse assumes a quick character from the greater facility the blood has for flow- ing centripetally. The wave is high, and the finger of the observer experiences a considerable stroke from it; but the very i moment after the expansion of the vessel the systole follows * extremely rapidly. It is this short duration of the diastole which gives such an exquisite impression of rapidity—of the celerity, which Corrigan first described, and in whose honor the French called it pouls du Corrigan. The sphygmographic tracing exhibits for aortic insufficience perhaps the most characteristic curves of all heart diseases, but it is most certainly not specific. The sharp line of ascension indicates the rapid and forcible dilata- tion of the wall of the vessel, since the lever of the instrument is raised with force, and falls at a very acute angle. The anach- rotous formation of small hooks in that part of the tracing which corresponds to the diastole of the vessel should be no more regarded as a result of some defect in the instrument than the sharp point of the summit. Besides, the tracings are not at all constant, They vary with the degree of hypertrophy and the strength of the left ventricle, and, further, they vary according as the aortic insufficiency is complicated with much atheroma of the INSUFFICIENCY OF TJIE AORTIC VALVES. 137 arteries, or produced by the endocarditic process alone. Further variations may be caused by a combination with stenosis of the orifice, or finally by a complication of mitral insufficience, which so often occurs from disease of the aortic flap. I intentionally print two sphygmographic tracings, which vary from the usual curve given by Marey. Marey's (Fig. 13) occurs most frequently, but they all have the sharp line of ascension in common. Fig. 13. Fig. 14. Aortic insufficiency with slight stenosis of the ostium and atheroma; especially characteristic are the steep ascending line, the marked formation of a hook or plateau, and the slight expression of the elevation for recoil. Fig. 15. Insufficiency of the aortic valves, accompanied by insufficiency of the mitral, and after the compensation has been deranged. Caused by endocarditis, as proved by the post-mortem examination. The tracing in Fig. 16 shows how little characteristic the "formation of booklets " (Hackchenbildung) or the sharp summit of the ascending line is for this definite valvular disease as such ; Fig. 1G. for here the former is very much more strongly expressed, though there was no valvular defect at all, and nothing but hypertrophy of the left ventricle in consequence of renal disease and sclerosis of the aortic system. 138 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. Also the great force with which the hypertrophied ventricle propels the abnormal quantity of blood into the aorta, may be recognized not only by the height of the pulse, but also by the fact that pulsation becomes visible in the smaller vessels, where before it was not even palpable. In the very capillaries, where pulsation is usually only seen under the most favorable circum- stances, it can be seen when the aortic valves are insufficient, as Quincke has demonstrated. Under these conditions, too, the spontaneous pulse has been seen by different observers in the branches of the retinal artery (comp. Becker). But this only occurs in highly-developed cases, and is more easily seen the more hypertrophied the left ventricle is. When the compensation is disturbed, the retinal pulsations also disappear. Even in the small vessels audible vibrations are produced in the rapid transition from a low to a higher tension. One can, for instance, hear a systolic sound on the volar arch, though only in extreme cases, while, even when the defect of the valve is but slight, a systolic sound may be heard on the large arterial trunks, especially the cruralis, the tension of which is greater than that of the carotid. This production of sound in the cruralis is, indeed, no specific symptom of the particular disease under con- sideration, since it can occur as well under other conditions, when the retreat of the blood during cardiac diastole is facilitated, as, for instance, when the tone of the vessels is low in fever or chlorosis ; still it is one of the most constant symptoms. There is another symptom to which special attention has been drawn by Duroziez, and which occurs on the cruralis. It too is not pathognomonic, but occurs most frequently in aortic insuffi- ciency. Duroziez found that if one pressed, whether with the stethoscope itself, or with the finger above and below the steth- oscope, on the crural artery, he would hear, not as usual, a simple systolic murmur, but a reduplicated murmur, both a systolic and a diastolic one. The latter is owing to the eddies which are produced in the blood during the diastole of the heart by the regurgitation of the centripetal wave through the artificially con- stricted lumen. Though this fact is very valuable and perfectly established through repeated observation, yet it only adds one to the number of symptoms of insufficience of the aortic valves. INSUFFICIENCY OF THE AORTIC VALVES. 139 But Traube has made us acquainted with a new symptom, which enables us to estimate the degree of insufficiency of closure in the valve. He demonstrated that when the insufficience was very great, a reduplicated sound, a systolic and a diastolic, can be heard on the cruralis without any artificial pressure. He explains the production of the sound from the fact that mem- branes begin vibrating audibly during a transition from a maxi- mum to a minimum tension. These conditions are best fulfilled by the crural artery, since its tension during the systole of the heart is abnormally great, and its slackness during diastole is very considerable, owing to the facility the blood has of flowing both into the capillaries and back towards the heart. However, we must here presuppose that the function of the left ventricle is undisturbed, and the vascular elasticity unimpaired. Otherwise this reduplicated sound may be absent, as in a case of atheroma which came under my observation. We comparatively seldom hear a patient make any subjective complaints so long as the hypertrophied muscle of the left ven- tricle can perform its work and propel its increased supply of blood with sufficient force into the arteries. As insufficiency of the aortic valves produces no injurious reaction in the pulmonary circulation till a very advanced stage, patients suffering from this disease are for a long time free even from shortness of breath, which is seldom quite absent when the mitral valve is insufficient even in the compensation stage, and almost never absent after exertion. But in the hypertrophy itself lies a source for evils, which too begin to work. The constant expansion and persist- ent pressure to which the vessels are exposed serve to produce a condition of congestion perceived by the tendency to hemor- rhage. It is more especially in the brain, where the compensa- tion of circulatory derangements is greatly hindered by the un- yielding auxiliary substance around the vessels, that fluctuations and agitations often assume a dangerous character, and annoy patients under the form of a beating headache, for the disturbed nutrition of the vessels (both etiologically connected with the valvular defect, and also being the result of a persistently high pressure) diminishes their power of resistance so much that death often results from hemorrhage into the brain. In this case both 140 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. factors combine, both the atheromatous process and the fatty de- generation of the small cerebral vessels, along with hypertrophy of the left ventricle. But there is a further symptom which annoys the patients—namely, a pain occurring spasmodically, situated beneath the sternum, of a constricting nature, and increased by exertion. It is often accompanied by an unspeakable feeling of terror, and is probably due to the simultaneous atheromatous process in the arch of the aorta and the irritation propagated from here to the cardiac plexus. Michel Peter records a case in which anatomical changes were found in the ganglia of this plexus after death, which goes to support his explanation of the symp- tom as we have just stated it. When the propelling force of the circulatory apparatus is impaired by disease of the hypertrophied cardiac and vascular muscles, all the signs of over-filling and stagnation appear in the venous system alongside of arterial anaemia. These signs have been already frequently mentioned. The patients become short of breath and dropsical; the peripheral cervical veins are expanded and over-filled. Most worthy of mention among the symptoms of disturbed circulation in the internal organs are the dizzy fits, which express venous hypergemia in the brain, and albuminuria, indicating renal cyanosis. In this connection we must not omit to mention the inflammatory processes in the nutrition of the kidneys, which are one of the most frequent complications of aortic insufficiency, even at an early period, before there is any stagnation whatsoever. It is erroneous to look for the origin of albuminuria, as some have done, in active congestion, since mere increase of pressure in the aortic system never produces albumen in the urine. The anatomical changes in the kidneys in cases of this kind point to interstitial nephritis, and must be regarded as a complication of the cardiac disease. Occasionally there occurs a striking paleness of the face, which we must connect with the simultaneous albuminuria. The diagnosis of aortic insufficiency can only be founded on the physical signs, the most definite of which are the diastolic murmur, with maximum intensity over the sterno-costal articu- lation of the third right rib and on the sternum, and, connected with this, dilatation and hypertrophy of the left ventricle. For INSUFFICIENCY OF THE AORTIC VALVES. 141 the other symptoms, as, for instance, the sounds in the arteries, especially in the cruralis, are not specific, and are not produced exclusively by the derangements in the circulation resulting from valvular disease, and consequently occur as well under other conditions, or may entirely cease when the compensation is disturbed, as in the case of the otherwise very characteristic pulse. In cases where doubts arise as to the signification of an audible diastolic murmur, especially where the mitral valve is involved, whether it is stenosis of the left ostium venosum or insufficience of the aortic valves (in the stage of disturbed com- pensation), apart from the diagnostic value of ascertaining the situation of maximum intensity of the diastolic murmur, great advantage may be derived from Duroziez's symptom of the "double souffle intermittent" in the cruralis, which occurs only in this one form of disease. Traube's symptom of the redupli- cated sound in the crural artery enables us to estimate the degree of insufficience when this is considerable and while the compen- sation remains undisturbed. As an insufficience, capable of producing this reduplicated sound, excludes any simultaneous stenosis of the ostium, the symptom obtains a new importance. The prognosis, as regards the length of life and activity of the patient, is more favorable in aortic insufficiency than in any other valvular disease. He may enjoy years of undisturbedly good health, as long as the increased force of the left ventricle suffices to prevent any stagnation of the circulation. It has been observed that disturbances of this course set in earlier, when the patients are young and the process originates in endo- carditis, than in old people with atheroma. As soon, however, as conditions appear which render the compensation imperfect, the reaction on the venous system takes place rapidly, and the whole cyclus of symptoms of stagnation leads far more quickly to a fatal termination than is the case in uncomplicated mitral disease. Special caution must be taken in the prognosis, when the patient exhibits signs of a disarranged intracranial circu- lation, in the form of dizzy fits, or, more unfavorable still, fainting-fits. The fear of the occurrence of apoplexy cannot be regarded as a mere bugbear, in spite of weighty protests against it, and it should be well taken into consideration in forming a 142 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. prognosis. It is to be apprehended more especially in cases which originate in an atheromatous process. Even when death does not occur from apoplexy, yet it is more frequently of sud- den occurrence in this than in the other valvular diseases. Stenosis of the Ostium Aorticum. The anatomical changes in the valves, producing stenosis of the orifice, consist chiefly of fibrous thickenings or calcifications of one or more flaps (sometimes all over and sometimes only at their base), and also lateral adhesions of the free borders. We generally find both changes occurring more or less together. When they are highly developed, the orifice is so constricted that only a narrow triangular split remains open, whereas in the normal condition it is large enough to allow the thumb to pass through it. In general, however, the stenosis of the ostium aorticum does not reach such an advanced stage as in the left ostium venosum. Just as in this latter case, on account of its anatomical cause, the insufficience was accompanied by stenosis, a similar relation is exhibited by the arterial ostium. It is only in the extremest cases of constriction, when the rigid flaps remain invariably expanded alike in systole and diastole of the ven- tricle, almost touching one another, that scarcely any blood can regurgitate into the ventricle during the diastole ; in such cases alone do we see exclusively stenosis. The mechanical effect, whether this be produced by alteration of the valves, or by myo- carditic changes in the pars aortica (a case of the very rarest occurrence), is always that the left ventricle has a difficulty thrown in its way which embarrasses its propulsion of blood into the aorta. If the power of the ventricle for the same unit of time remain the same, it cannot propel all the blood brought to it from the pulmonary veins through the constricted orifice. Consequently less blood must get into the aorta, and a positive quantity corresponding to this minus must accumulate in the left ventricle. This ventricle is dilated, and its muscle increases in proportion to its greater tension, so that its higher propulsive force overcomes the disturbance in the circulation. Accordingly, STENOSIS OF THE OSTIUM AORTICUM. 143 the secondary changes we find in the heart itself are dilatation and hypertrophy of the left ventricle. Theexcentric hypertrophy, namely, that in direct proportion to the dilatation, is the more pronounced the greater the tension undergone by the ventricle. It is consequently greater if the stenosis be accompanied by in- sufficience of the valve than without this ; whereas, even in the most extreme cases of pure stenosis, the dilatation is thrown into the shade by hypertrophy, as is plainly demonstrated by Bamberger's measurements. Since death seldom occurs before the compensation has been destroyed by disease of the cardiac muscle or otherwise, we generally find the result of this in the shape of a dilated left auricle and right side of the heart. For, as soon as the blood accumulated in the left ventricle can no longer be propelled forwards by the stronger exertions of this hypertrophied muscle, the already abnormally high pressure in the pulmonary venous system must be propagated through the pulmonary branches into the right side of the heart, and thus compel this to take part in the compensation. The peripheral arteries and the aorta itself are found to have abnormally small lumina, in proportion to the small quantity of blood which flowed through them in the same unit of time. The chief physical signs which the patients exhibit during life are increase of the volume of the heart, and especially dila- tation and hypertrophy of the left ventricle; but these are sub- ject to variation, more particularly according to the degree of simultaneous insufficience of the valves. "When stenosis greatly preponderates (the case now under our consideration), the area of cardiac dulness, as ascertained by percussion, is found to be moderately enlarged in its long diameter, below, and to the left. On the right the boundaries of dulness are generally nor- mal. The apical impulse is quite different from what we see in insufficience of the aortic valves ; it does not raise a large area and make it vibrate ; on the contrary, it is often weak, and may frequently be even quite imperceptible. Traube' has explained this striking fact by pointing out that one of the factors in the cardiac impulse, that is, the force of recoil or the power which drives the heart in the direction opposite to the systolic outflow, is impeded in stenosis, since the size of the aortic opening is 144 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. smaller, and the resistance to the outflow greater, than under normal conditions. In auscultation we generally hear a systolic murmur and a weak diastolic sound over the apex of the heart. When the valves are at the same time insufficient, we may hear a diastolic murmur as well. This systolic murmur is of a sawing, whistling character, occasionally musical; it grows louder as one nears the articulation of the third left costal cartilage with the sternum, and reaches its maximum intensity to the right of the sternum at the sterno-costal articulation of the third right rib ; but it can generally be heard so loud all over the heart that it is difficult to assign its situation of maximum intensity. The second dia- stolic sound is quite absent, or only slightly audible. The same may be found in the case of the carotids, where too we hear a loud systolic murmur and no second sound. The state of the pulse is of as much importance as the results of auscultation, for it is distinguished by two characteristics peculiar to this valvular disease. Though the lumen of the radial artery remains normal, the pulse is strikingly low, while the tension is normal or even slightly increased. Besides its small- ness and hardness, the pulse is remarkable for its slowness. The explanation of all this is very simple; the wave is low, because even the hypertrophied left ventricle can only propel the nor- mal quantity of blood through the narrow orifice of the aorta by prolonging its systole; and thus the wave is made longer. Its slowness is due to the smaller number of contractions in the same unit of time, and this again is due to the abnormal length of each systole. That the systole is much longer, may be seen from such a sphygmographic tracing, as the one we give by Fig. 17. Marey, taken from a left ventricle still capable of work. Here the abnormal length is shown in the rounded top, almost forming a plateau, and in the long descending line. However, these tracings vary with the force of the left ventricle and the degree STENOSIS OF THE OSTIUM AORTICUM. 145 of complication by insufficiency of the valve ; so it cannot be regarded as specific for all cases. As soon as the working power of the left ventricle begins to be incapable of overcoming the resistance caused by the stenosis, the pulse grows smaller and strikingly soft. In this case, too, when compensation is deranged, the symp- toms of stagnation are developed in the different organs. In the lungs the altered condition of the circulation causes the patients to complain of dyspnoea, which occurs in fits, sometimes ac- companied by appearances of catarrh, sometimes in the form of purely so-called stenocarditic attacks. But the stagnation here often gives rise to genuine haemoptysis, corresponding to which apoplectic centres or hemorrhagic infarctions are found in the post-mortem examination of the lungs. Anaemia in the brain produces fits of faintness and dizziness, which generally occur suddenly. It may happen, too, that the nervous derangements exhibit quite a peculiar picture. In apparently good health, for instance, all the joints relax, so that the patient gives one the impression of a person sleeping calmly in a sitting posture ; he retains consciousness, but has no command of motor power. In other cases, genuine epileptic fits may be observed. There are no special difficulties attached to the formation of a diagnosis, when all the physical signs are present, and when attention is paid as well to the condition of the pulse with its smallness and hardness, as to the auscultatory symptoms. The systolic murmur, indeed, with its greatest intensity over the third right sterno-costal articulation, can originate in disease of the ascending aorta as well as in mere roughnesses on the flaps of the valves. However, the simultaneous absence, or at least strik- ing weakness of the second sound, and the accompaniment of a small, hard, slow pulse, when present, insure against any such con- fusion. But when the left ventricle's force is impaired, the char- acteristic hardness of the pulse may completely disappear, leaving only its smallness. In this case we should remember Forget's accurate remark : "La petitesse du pouls est un signe banal, qui n'a de valeurque lorsqu'il est joint a la durete, laquelle indique la force de contraction du ventricule gauche." For the auscul- tatory sign of the systolic murmur over the aortic ostium, with VOL. VI.—10 146 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. merely a small pulse, even with perceptible hypertrophy of the left ventricle, does not justify us in assuming the presence of stenosis. The absence of the apical impulse materially supports the diagnosis, when the other signs are present, but only after the exclusion of all other forces which could render the impulse invisible. The prognosis as to the duration of the affection is in so far favorable as the disease may last a long time without impairment of the general health and activity, until the compensation begins to fail. But, when the stenosis is extreme, the symptoms of disturbed compensation appear far sooner than in a case where insufficiency of the valves predominates, and, compared with this latter, the prognosis of stenosis is not nearly so favorable. But, if we compare the prospects of stenosis of the ostium aorticum with those of stenosis of the ostium venosum sinistrum, the prognosis of the former is far more favorable as regards the duration of life. Valvular Diseases of the Right Side of the Heart. Allan Burns, On some of the most frequent and important heart diseases; chapter on pulsation in the epigastric region.—Friedrich Cramer, Die Krankheiten des Heizens. Cassel, 1837. Anmerkung iiber die Venenpulsation, p. 50.—Knabe (Traube), De venarum intumescentia atque pulsatione. Diss. Berol. 1853.— Ch. Bernard, Quelques remarques sur les lesions valvulaires des cavites droites du cceur. Arch, gener de m£d. 1856.—Roth, Falle von Insufficienz der Tricuspidalklappe. Baier'sches Aertzl. Intelligenzblatt. 1858.—P. Guttmann, De insufficientia valvulse tricuspidalis.—Berol. 1858.—Kolisko, Fall von Insufn- cienz der Tricuspidalklappe. Zeitschr. der Wiener Aerzte, 1859.—Bamberger, Beobachtungen iiber den Venenpuls. Wiiizb. med. Zeitschr. 1863.—Geigel, Ueber den Venenpuls, ibid. 1863.— The same, Weitere Beobachtungen iiber Tricuspidalinsufficienz und Venenpuls, ibid. 18(5.— Ilaldane, Case of disease of tricuspid valve. Edinb. Med. Journal, 1864.—M. Seidel, Ueber Pulsation der Vena cava inferior. Deutsche Klin. 1865.—Friedreich, Ueber den Venen- puls, im Deutsch. Arch. f. klin. Med. 1866.—Bouger, De l'insuffisance de la valvule tricuspide. These, Paris, 1866.—Mahot, Des battements du foie dans l'insuffisance tricuspide. Paris, 1869. Insufficiency of the Tricuspid Valve. The anatomical changes which produce incapability of clos- INSUFFICIENCY OF THE TRICUSPID VALVE. 147 ure in the tricuspid valve, just as in the mitral, originate almost solely in endocarditic processes. Very rarely, indeed, are cases seen of myocarditis involving the septum and forming abscesses, which burst into the ventricle, and thus give rise to the rupture of a flap from its insertion. In such cases insufficience exclusively is produced ; but in cases, too, where the endocarditic changes lead simultaneously even to a slight adhesion of the flaps, the accompanying stenosis of the orifice is extremely trifling. Disease of this valve nearly always begins during foetal life, and seldom occurs as an independent affection in adults—in fact, out of a hundred cases of cardiac valvular disease, scarce two occur in the tricuspid; and even in these few cases the tricuspid is generally not the only affected part, being nearly always accom- panied by disease of another valve, usually of the mitral. But the form of relative insufficience, described by Gendrin, occurs more frequently than that which is due to shrinking and thicken- ing of the borders of the valves. Hindrances in the lesser circu- lation, whether from affection of the lungs themselves or from stenosis of the left ostium venosum, produce an accumulation of blood in the right ventricle. This dilates the ventricle very considerably, so that the ring of insertion of the tricuspid becomes larger, so much so that the flaps, though very slightly, if at all, anatomically altered, are rendered insufficient for the closure of the orifice. All arguments which have been brought against the possibility of this relative insufficiency are founded mainly on the fact that the flaps of the tricuspid are so long that one of them would suffice to close the normal ostium. But these arguments will not stand testing, and have been refuted by different investigators, most thoroughly by Friedreich, whose measurements have put it beyond doubt that even the height of the tricuspid flaps may be too small for the enlarged circum- ference of the ostium. Besides, clinical appearances prove the presence of a relative insufficiency with the greatest certainty. The mechanical result of this valvular defect consists of regur- gitation of blood into the right auricle during every ventricular systole. The auricle is consequently dilated and hypertro- phied, too, in proportion to its slender muscle. The tension in the venae cava3 must rise considerably, whilst that of the pulmonary 148 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. artery and aortic system falls. Just as we saw the left ventricle dilated and somewhat hypertrophied in insufficience of the mitral valve, where the filling took place under high pressure, so here we see the right ventricle dilated and hypertrophied, since it, too, is filled during diastole under extra pressure. This change in the ventricle is the only one directly connected with the affection of the tricuspid, but not the only change we may observe. Other changes may take place in the left ventricle, chiefly the result of mitral affections which are present at the same time, and these are naturally not without their influence on the degree of dilatation and hypertrophy of the right ven- tricle. The physical symptoms, in the majority of cases, indicate a complicated affection of the heart, and we must accordingly in each case separate the signs of tricuspid disease from those of others simultaneously present. Inspection and palpation always indicate an extension of the cardiac impulse to the right. In percussing we find the area of cardiac dulness enlarged chiefly in width; when the right lung is not at the same time hypertrophied, a dulness is most strikingly audible on the right of the sternum between the fourth and second ribs, correspond- ing to the dilated auricle. Alterations of the figures of absolute and relative dulness to the left only occur when changes are at work at the same time in the valvular apparatus of the left ventricle, resulting in the development of changes of volume of the left ventricle. In auscultation we may hear a blowing murmur over the lower segment of the sternum, synchronous with the cardiac systole, and reaching its point of maximum intensity on the right border of the sternum, between the fourth and fifth ribs. This is to be regarded as a symptom of an affec- tion of the tricuspid. On account of the mitral affection which accompanies nearly every case, we hear a systolic or diastolic murmur over the cardiac apex, according as insufficience or stenosis of the bicuspid preponderates. The second sound is weak over the right side of the heart, where we hear it as trans- mitted from the pulmonary artery. On this artery itself, too, both sounds are weak, on account of the emptiness which prevails in it during this valvular disease. Still the symptom may be INSUFFICIENCY OF THE TRICUSPID VALVE. 149 modified in another direction by the presence of a mitral affec- tion. The aortic system receives less blood than normally, in consequence of the empty condition of the pulmonary artery, and so the radial pulse feels very low. But no further varia- tions can be detected in it. On the other hand, on the visible veins of the neck, and, first of all, on the bulb of the internal jugular vein, then along the whole vein itself, and later also on the external jugular, we can see and feel a pulsation quite plainly in the majority of cases. Even before the cervical veins begin to pulsate we may observe the phenomenon in the liver. Here its occurrence is attended with less difficulty than in the veins of the neck, since the hepatic veins possess no valvular apparatus which could hinder the regurgitation of blood. For, as we have already explained in the general introduction, the venous pulse in the neck is never visible and palpable until the valves of the veins are incapable of closure, in addition to insufficience of the tricuspid valve. When there is no insufficiency of the venous valves, the pulsation only occurs in the bulb of the vein, and not along its whole course in the neck; while in the liver it is perceptible at an earlier stage, on account of the absence of the above condition. When the pulse is confined to the bulb, and the valves are unimpaired, a sound is produced by the vibrations from their closure. This "sound of the jugular valves" was first remarked by Bamberger, and is of great diagnostic value for those cases of tricuspid insufficiency where we cannot per- ceive any pulsation on the venous bulb. The venous pulse in both the neck and the liver may appear and disappear succes- sively in the course of the disease. All forces which tend to diminish the stagnation in the venae cavse, or lessen the quantity of blood in the body, or reduce the propulsive force of the right ventricle, may make the venous pulse in the neck disappear ; on the other hand, quite local influences, as, for instance, an accu- mulation of serum in the peritoneum and the change in the liver's position produced by this, may render the hepatic pulsa- tion for a short time invisible, but it returns immediately after puncture. Under favorable conditions the vena cava in- ferior, as Geigel has demonstrated, may be seen and felt as a pulsating vessel even in the right mesogastric space. All further 150 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. details regarding the venous pulse need no repetition here, as we entered so fully into them in the general introduction. Functional disturbances occur here at an earlier stage than in the left ventricle, for the compensatory action of hypertrophy in the right auricle, owing to its slight muscularity, is very trifling, and the increase of volume of the right ventricle has generally to do duty for the mitral affection. Consequently all the symp- toms of stagnation, such as dropsy and cyanosis, appear early in the course, and are never absent. The pulmonary circulation, too, suffers some derangement both at the commencement, since the pulmonary artery is not normally supplied, and also later, when there are numerous coagula formed in the right auricle and ventricle, giving rise to stagnation and infarction. The diagnosis is rendered specially difficult by the simul- taneous presence of mitral disease. It is particularly important not to be deceived by murmurs transmitted from the mitral orifice. In this respect an accurate discrimination of the timbre of the murmur is of great service. The diagnosis may be estab- lished with certainty when we see a plain and vigorous pulsation in the cervical veins or in the region of the liver, in conjunction with a systolic murmur between the sternal insertions of the fourth and fifth ribs, and a weak second sound over the pulmo- nary artery. The prognosis is unfavorable on the mere grounds we have mentioned, even if the tricuspid affection were completely un- complicated ; and it is all the worse, as this valvular disease sel- dom develops before others are already in action. Stenosis of the Ostium Venosum Dextrum Stenosis of the right venous ostium occurs still more rarely than insufficiency of the tricuspid valve, and when it does occur it dates from foetal life, and, one may say, always is accompanied by some other cardiac affection, especially one of the left venous orifice. The anatomical change which produces the constriction, too, is similar to that of the left side which we have already described. In examining the heart, we find as the result a con- siderable dilatation of the right auricle, and hypertrophy of the STENOSIS OF THE RIGHT OSTIUM VENOSUM. 151 right ventricle generally, as the venous ostium of the left side is usually constricted at the same time, but the left ventricle is usually atrophied. Still, we must not forget that the condition of the left ventricle is also dependent upon simultaneously occurring disease of other valves, and may, accordingly, in some cases be found hypertrophied. This was the case in an instance observed by Forget, where the aortic ostium was constricted. He found the left ventricle considerably dilated and hyper- trophied. Since a stenosis completely confined, to the right ostium is not recorded, the physical signs correspond to the complications. Percussion proves an extension of the areas of absolute and rela- tive dulness in the transverse diameter of the heart, indicating chiefly hypertrophy of the right auricle. In auscultating we actually hear a number of murmurs, from which we must isolate those that point to stenosis. It is consequently merely a rule derived from theory which states that a diastolic or presystolic murmur is heard on the right border of the sternum, about the fourth rib. In a case where the ostium was only wide enough to admit the point of the little finger, Hope could perceive no murmur at all. This will cause less astonishment when we con- sider that the same has been observed of the mitral orifice; both may be explained on the ground of weakness of the circulation. Theory would also require a strikingly weak second sound in the pulmonary artery, owing to its small contents. Yet the presence of other valvular diseases may render this symptom, too, illusory. The appearances on the cervical veins, notwith- standing the tricuspid insufficience always connected with stenosis, are not necessarily^ so prominently expressed as in a case of the valvular disease alone, where the force of the hyper- trophied right ventricle comes into play. And it is probably an error on Kreyssig's part to state that both the cervical veins and liver pulsate most strikingly in stenosis. Others state that the symptoms are wholly absent; but this is most distinctly dis- proved by a case which Burns records. It is absurd to mention any compensation that may take place in this disease, for this must be derived solely from the right auricle, the muscle of which, even when hypertrophied, is insufficient. All symptoms 152 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. of venous stagnation, such as dropsy, cyanosis, etc., are ac- cordingly quickly developed, and soon lead to a fatal result. The diagnosis would be easily established if the constriction of the right venous ostium were the only valvular disease we had to deal with. But the isolation of the symptoms from those of the other diseased valves renders the task very difficult. Theoretically, we should lay most weight on a diastolic or pre- systolic murmur, which reaches its maximum intensity over the fourth sterno-costal articulation, and which can be distinguished by its timbre as one that has not been propagated from the left ostium. Besides this, as Hope's observation shows, there may be no murmur in stenosis at all, and this deficiency is no proof against the presence of the disease. The great scarcity of actual observations does not as yet allow of an exhaustive treatment of the diagnostic possibilities. The prognosis is even more unfavorable than that of prepon- derating insufficience. Diseases of the Valves and of the Ostium of the Pulmonary Artery. In addition to the handbooks we have given, consult: Norman Chevers, Recherches sur les maladies de l'artere pulmonaire. Archives ggn6r. de ingd. 1847 (extract from the London Med. Gaz. 1846).—Benedict, Fall von Insufficienz der Valv. semi-lunar. Arter. pulmonal. Wiener Wochenschr. 1854, No. 35.—Frerichs, In- sufficientia valv. Arter. pulmon. etc. Wiener Wochenschr. 1853.—Stanhope Templeman Speer, Case of cyanosis with extreme contraction of the orifice of the pulmonary artery. Med. Times, 1855.— H. Meyer, Ueber angeborene Enge der Lungenarterienbahn. Virch. Arch. 1857.— Whitley, Cases of diseases of the pulmonary artery and its valves. Guy's Hosp. Rep. 1858.—Kolisko, Fall von Insufficienz der Pulmonalarterienklappen. Zeitschrift der Wiener Aerzte 1859.—v. Dusch, In Verhandlungen des naturhistor. Vereins zu Heidelberg, 1859.— v. Wahl, Acute Endocarditis der Pulmonalklappen. Petersb. Med. Zeitschr. 1861.—Klob, Beitrage zur Pathologie der Pulmonalarterienklappen. Zeitschr. der Wiener Aerzte, 1861—//. Lebert, Ueber den Einfluss der Stenose des Conus arteriosus des Ostium pulmon. auf Entstehung von Tuberkulose (the older records of cases may, too, be found here). Berl. klin. Woch. 1867.__ Kappeler, Stenose der Arteria pulmonalis. Arch. f. Heilk. 1863.—Mannkopf, Ueber Stenose des Ostium arteriosum der rechten Herzkammer. Berl. Charitg- Annalen. 1863.—H. J. Halbertsma, De afwijking van het tusschenschot, etc. Ned. Tijdschr. voor Geneesk. 1862. —Brondgeest, Over pathol. veranderingen INSUFFICIENCY OF THE PULMONARY VALVES. 153 der Arteria pulmonal. enz. Nederl. Archief. voor Geneesk. en Naturk. 1864. —Karl Stalker, Ueber angeborene Stenose der Arteria pulmonalis, Bern. 1864. —Kussmaul, Ueber angeborene Enge und Verschluss der Lungenarterie. Zeitschr. f. rat. Med. 1865.—van Veen (Rosenstein), Over Stenose van het Ostium der Arteria pulmonalis. Gron. 1870.—Roeber, Ein Fall von Insufficienz der Pulnionalklappe. Berl. klin. Woch. 1870.—H. Meyer, Mittheilungen aus den pathol.-anatom. Demonstrationen von Buhl. Baier'sches Med. IntelL-Blatt, 1870.—Const. Paxil, Du retrecissement de l'artere pulmonaire contractee apres la naissance, etc. Union medic. 1871. Nos. 97-112.— Chr. Fengcr, Stenose of ostium pulmonale, etc., aus Nord. Medisk. Archiv (Refer, in Virchow und Hirsch. Jahresber. 1874). Insufficiency of the Pulmonary Valves. Whilst insufficience of the right venous ostium is almost un- exceptionally found to be accompanied by disease of some other valve, insufficience of the pulmonary valves occurs more inde- pendently ; it may also be acquired after birth, though exceed- ingly rarely, and thus it does not originate solely during fcetal life. Both the endocarditic and the atheromatous processes give rise to the anatomical changes in the valves, consisting mainly of shrinking and thickening of the free border. Wahl has observed cases in which the valvular flap was almost com- pletely destroyed by acute endocarditis. In the small number of cases as yet recorded we find one where the flap of the valve was ruptured at its insertion, after perforation of the septum by myocarditis, and thus insufficience was produced; and in two cases occurred the rare anomaly of a superfluous flap, which was either atrophied or totally annihilated (Kolisko, Klob). Under the last-mentioned conditions the case is one of pure insuffi- cience, whereas in all other cases there is generally more or less stenosis at the same time. The same mechanical results of the valvular disease prevail for the right ventricle as for the left in insufficience of the aortic valves. Accordingly, where the defect has lasted long enough to allow the development of the secondary symptoms, dilatation and hypertrophy of the right ventricle and auricle are observed. As the consequence of this, and harmon- izing with the conditions in aortic insufficiency, we find the pul- monary artery dilated, both trunk and branches, and along with this Ave see signs of deranged nutrition on the Avails of this 154 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. vessel. When the aortic valves are at the same time affected, results of this are found in the left ventricle; whereas it is other- wise always atiophied, as may easily be imagined from the small quantity of blood it receives. At the post-mortem examination less blood than usual is found in the lungs, even when the mitral valve as well is insufficient, as in one case recorded by Klob. But this does not justify Kolisko in excluding the possi- bility of a temporary hyperaemia during life. The quantity of blood is in reality dependent on the degree of stenosis accom- panying the insufficiency, and also on the secondary hypertrophy of the right ventricle. Both the lobular patches of pneumonia, which are repeatedly found, and also the hemorrhagic infarc- tion, testify to increased pressure existing in the pulmonary vessels at the time of compensation. As physical signs we may recognize: enlargement of the volume of the heart, found by percussion, chiefly towards the right; in auscultating, a diastolic murmur, which reaches its maximum intensity on the left border of the sternum between- the second and third ribs. This murmur is very loud, and can be heard also over the inferior part of the sternum, as it is propagated towards the right ven- tricle in the direction of the current which produces it. On the other hand, it cannot be propagated along the course of the large cervical vessels, and is never heard over them. A second sound is sometimes heard as well as the diastolic murmur, but this depends on the degree of capability of vibration which a part of the valvular flap may retain. Instead of the first sound, we hear a systolic murmur, which may originate in the transi- tion of the current into the dilated trunk of the vessel, and, consequently, cannot always be regarded as a sign of the presence of stenosis, though it may arise from this in some cases. The subjective complaints of the patient relate chiefly to impeded respiration and palpitations of the heart, according to the over-filling or emptiness of the pulmonary vessels at the time. Neither of them, however, is severe ; on the contrary, the course of cases on record shows that hypertrophy of the right ventricle is capable of compensation for a comparatively long time. The non-closure of the foramen ovale, which we often find in company with this valvular disease, contributes favor- STENOSIS OF THE PULMONARY OSTIUM. 155 ably here, in as far as it allows blood to flow from the already overfilled right auricle into the left. By this means stagnation in the venae cavse is avoided, and, besides, it helps to fill the left ventricle. It is not before the compensation begins to fail, sloAvly and gradually, as we have observed, that very marked cyanosis, swollen cervical veins, and dropsy, etc., set in. The prognosis is unfavorable as regards the final result. How- ever, if we may draw conclusions from the exceedingly limited number of cases on record, the length of a patient's life, who is suffering from insufficience of the pulmonary valves, may be comparatively long. Stenosis of the Ostium of the Pulmonary Artery, An alteration of the ring of the valve, and of its flaps, by the endocarditic or atheromatous process, is acquired so very seldom after birth, that the whole literature only contains a few isolated cases (Whitley, Speer, Mannkopf), to which I can add my own, described by van ATeen in his dissertation. Such an alteration can, like the process on the aortic valves, produce so marked constriction of the orifice, as to figure as the only, or at least very preponderant, derangement. All the other obser- vations, even those regarding this valvular disease as one ac- quired after birth, were concerned with a combination of stenosis and a very considerable degree of insufficience (Frerichs, Bene- dict, etc.). When the stenosis is acquired after birth, it is chiefly produced by adhesion of the free borders of the valvular flaps, with or without simultaneous atheromatous thickening of their bases, and can reach such a point that it is impossible to pass a thin catheter or, as in Speer's case, a quill through the opening. In the case Avhich came under my own observation, the atheromatous thickening was completely confined to the base of the valvular flap, while the trunk and branches of the pulmonary artery Avere quite free from it. Besides this, I only found a small opening in the position of the foramen ovale, two millimetres in diameter; the septum ventriculorum was per- fectly closed, likewise the ductus Botalli. Though the patient did not come under my observation till he was thirty-three years 156 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. old, and had, from early childhood, exhibited signs of dyspnoea and cyanosis, still, the fact that all the foetal passages had closed, justifies me in asserting that the disease was acquired after birth. The small opening of the foramen ovale may be regarded as within normal limits. Since a comparatively old age (up to thirty years and more) may be reached by a patient with con- genital stenosis of the pulmonary ostium, which occurs incom- parably oftener than the acquired, the question to decide, whether in each special case Ave are dealing with a congenital or an acquired cardiac affection, is not always an easy one, especially when we have not been previously acquainted with the patient. The most distinguishing characteristics of the two are as follows : the con- genital stenosis always originates in a number of anatomical changes, chiefly in the trunk of the artery, which is itself con- stricted in consequence of constriction of the conus arteriosus by myocarditic formations; the congenital, too, may be accom- panied by an affection of the valves, whereas a stricture confined to the latter alone, induced by foetal endarteritis, is very rare; acquired stenosis nearly always depends on endocarditic or atheromatous changes in the valves or in the valvular ring alone. Further, in the congenital form we always find a number of ana- tomical anomalies of the heart and blood-vessels, especially an unclosed foramen ovale (in sixty-four out of eighty-two cases, according to Stolker' s statistics), and a deficiency of the septum ventriculorum. This latter is always displaced to the left, and exhibits one opening of more or less importance, or else is not at all closed above. This deficiency in the septum is correctly regard- ed by H. Meyer as a result of the stenosis, and not the cause of it, as Heine asserts ; nor can the two be regarded as co-ordinate, ac- cording to Halbertsma's vieAv. Still it must not be denied that some cases confirm Halbertsma in regarding the defect of the septum, and the anomaly of the pulmonary artery, as co-effects of the original hindrance. The origin of the aorta from both ventricles, or even from the right alone, has often been observed in connection with a septum both deficient and displaced to the left. The ductus Botalli is found sometimes open and sometimes closed. According to Stolker's statistics, in sixty-nine cases, where this point was accurately examined, the ductus Botalli STENOSIS OF THE PULMONARY OSTIUM. 157 was thirty-eight times closed and thirty-one times open. Its remaining open is easily explained by the over-supply of blood in the aorta, consequent on constriction of the pulmonalis, as the lungs must now continue to be supplied by this foetal channel. In the cases where the duct was closed, the closure must have taken place at a stage in foetal life when the lumen of the pulmon- ary artery was still large enough to transmit a current sufficient for the lungs. When the ductus Botalli is closed, or when this channel is no longer quite capable of transmitting enough blood after respiration has commenced, we see the arteriae bronchiales, branches from the aorta, and sometimes also the arteriae oesoph- ageal and coron arise anteriores, dilate to form a collateral circula- tion, Avhich supplies the lungs by anastomoses between these arteries and the pulmonalis. But whether the constriction be congenital or acquired, the right ventricle, auricle and auricular appendix are found almost unexceptionally dilated and hyper- trophied, and the whole heart is more globular than usual, and lies transversely. The substance of the right ventricle may increase to such a degree, that it equals, and sometimes exceeds, the volume of the left. In the case Avhich came under my observation, the wall of the left ventricle measured 1.5 cm. at the base, and that of the right 1.1 cm. The left ven- tricle is always relatively small, though absolutely it may be of the normal size. The condition of the pulmonary artery beyond the stricture is variable, but, as a general rule, Ave may say that it is narrow in the congenital, but normal, or even dilated, in the acquired form. In the majority of cases, the branches beyond the bifurcation are dilated. The lungs are generally anaemic, and frequently contain caseous products or tubercles. The physical signs of acquired stenosis of the pulmonary artery are : an extension of the area of dulness to the right, extending beyond the right border of the sternum. The dulness may also extend to the left, owing to the more horizon- tal position of the heart. In auscultating we hear a systolic bloAving sound, which reaches its maximum intensity on the left border of the sternum in the second intercostal space, and spreads considerably to the left, but never to the right or into the large cervical vessels. The second sound in the pulmonary 158 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. artery is very weak, and may be quite inaudible sometimes. A systolic vibration may often be felt, though not invariably, in the situation of maximum intensity for the audible murmur. When at the same time the valves are insufficient, we hear a diastolic as well as the systolic murmur. The subjective condi- tion of the patient is usually undisturbed as long as his activity is not specially taxed. But with active physical exercise, or the occurrence of any acute disease, whether of the heart itself, or of the respiratory passages, especially diffuse bronchitis, severe dyspnoea is produced, and more or less intense cyanosis follows; on the other hand, the dropsical swellings do not occur till a later stage. These latter, and stagnation in the glandular or- gans of the abdomen, do not set in till the compensation of the hypertrophied right ventricle has been destroyed by degenera- tion of the cardiac muscle or by other forms. The physical signs in congenital stenosis of the pulmonary artery, as far as accurate descriptions go, and judging from three cases which have come under my own notice, seem to be the same as in the acquired disease. Only the development of hypertrophy of the right ventricle in early youth, while the thorax is still elastic, leaves a more marked impression on the chest, and the cardiac region is more arched. The cardiac im- pulse is weak and diffuse. The thinness of the child's chest, too, and its smaller extent, explain the fact that the intensity of the audible murmur and palpable vibration is far greater and further extended over the thorax in children than in adults. It is consequently extremely difficult to localize the murmur, for we can hear it over the whole cardiac region, and can even follow it into the cervical vessels. From some observations that have been made, it seems probable that stenosis of the pulmon- ary artery may occur without any abnormal murmur at all. To explain such cases as these, we must assume that the intensity of the circulation was not great enough to produce a murmur. In the majority of cases of children (according to Stolker, thirty- two out of fifty-seven, immediately after birth), cyanosis Avas quite noticeable from the very beginning, and especially during crying, not only in the face, but also on the hands and feet. But even where the cyanosis is not visible, or is absent owing to the STENOSIS OF THE PULMONARY OSTIUM. 159 quiet life led by the patient, yet it is generally quite striking after physical exertion. However, there are exceptional cases, in which either the first years of life run on without any derange- ment, and cyanosis does not occur plainly till the patient has grown somewhat, or else the subjective symptoms of a cardiac disease do not appear till the twentieth or thirtieth year. In such cases the collateral circulation probably sufficed, in conjunction with the unclosed foetal channels, to compensate the derangement till further deA-elopment of the lungs demanded a larger supply of blood, or neAv endocarditic processes rendered the existing com- pensation insufficient. These latter may occur at any time, and so, too, relatively late. The absence or presence of cyanosis is always dependent upon the degree of stagnation in the veins and capillaries. When the compensation is sufficient, there may be no cyanosis at all, but it sets in at once when the compensation is defective; and when it is gradually deranged, cyanosis slowly develops. The low temperature Avhich is objectively perceptible on the hands and feet of these patients, and is always remarked by them,'is connected with stagnation and insufficient oxidation of the blood. Even when there are no other s}Tmptoms, the little patients long for Avarmth, and cannot endure a cold wind very well. Small children sometimes have paroxj^sms of asthmatic breathing. In slightly older cases the characteristic symptoms of caseous pneumonia have often been observed proceeding from the lungs, and especially after haemoptysis and hectic fever. Sometimes children have crying fits, accompanied, too, by con- vulsions. In a case I had of a one-}Tear-old child, these convul- sions grew to actual epileptic attacks. The crying fits sometimes seem to result from painful paroxysms of coughing, but occur, too, independently of these. Children who exhibit these symp- toms die very soon. We may also see signs of a deranged cerebral circulation, especially attacks of dizziness and fainting, in children who have outlived the first few years. Besides this, in most cases of congenital stenosis, though not in all, Ave have an effect produced" on the general constitution. Bodily develop- ment is in many Avays baclvward, the bones are soft, the muscles weak, the subcutaneous fat insignificant, and the whole appear- ance of the patient generally does not correspond to his age. 160 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. But cases occur, as one of a boy twelve years old, who lately came under my care, where the cyanosis, setting in with physi- cal exertion, alone points to a heart disease, while otherwise the general constitution is quite strong. When the physician has known the patient before he acquired the stenosis of the pulmonary orifice, and if the physical symp- toms already described develop under his eyes, then the diag- nosis of the disease is not difficult. Under such conditions, there are only two cases in which there is any great difficulty in recog- nizing the disease. It may be accompanied, as I have seen it, by emphysema, especially in the right lung, and thus the lung may cover the heart so much that we can no longer ascertain its hypertrophy by the extension of the dulness to the right. In a case of this kind, besides the audible systolic murmur, which one might be tempted to regard as accidental, special weight should be laid on the weakness, or absence, of the second sound in the pulmonary artery. This sound can indeed become weak from fatty degeneration of the once hypertrophied right ventricle, even without the presence of emphysema ; but in this case we have other signs of stagnation expressing the derangement of compen- sation, especially symptoms of dropsy, which are the very last to come in this acquired stenosis. A second difficulty lies in the combination of insufficience with stenosis. Under these condi- tions the diastolic murmur may be very loud, and either conceal the systolic, so that this can no longer be heard at all, or, if it is heard, it is more likely to be attributed to vibrations of the wall of the vessel itself than to stenosis. This latter confusion, how- ever, has no practical importance. But of course no one would found a diagnosis on the presence alone of a systolic murmur in the neighborhood of the ostium of the pulmonary artery, since accidental murmurs, and others caused by compression, often occur here. When the murmur is accompanied by a palpable vibration, it gains greater importance. Confusion with stenosis of the aortic ostium is prevented by the extension of the murmur to the left, and by its not being propagated into the cervical ves- sels, and also by the perfectly normal condition of the pulse. The diagnosis of congenital stenosis of the pulmonary artery is greatly strengthened if, in addition to finding the physical COMBINATION OF VARIOUS VALVULAR AFFECTIONS. 161 signs, we ascertain from the history of the case that more or less cyanosis was observed at the birth of the patient, or was devel- oped immediately afterwards. But the absence of cyanosis does not at all exclude the congenital nature of the disease. Still the conclusion, as to its being congenital or not, can never be more than a probability, especially Avhere there is no cyanosis ; all the more so, as in some cases doubt may still exist after the post- mortem examination, even when the foramen ovale is found un- closed. The prognosis is so far unfavorable that old age is never reached by any case of this stenosis, whether congenital or acquired. The majority of congenital cases end in an early death. According to Stolker s statistics, 42 out of 99 cases died before their tenth year, and only 15 per cent, survived the age of twenty. Tuberculosis and caseous processes in the lungs figure prominently among the causes of death in the cases which lived to the age of twenty. Stolker calculates this to occur in 14 per cent.; Lebert's estimate is still higher. Combination of Various Valvular and Ostial Affections. In describing the individual valvular and ostial affections, we explained how the anatomical changes Avere generally of such a nature that on one and the same valve insufficience and stenosis of the ostium went hand in hand. Insufficience of the valves can, indeed, occur alone, but, as a matter of fact, it is only isolated in the rarest instances; while stenosis is always accompanied by insufficience, except in the worst developed cases, where, strictly speaking, the insufficience is so small, in comparison to the ste- nosis, that it is not taken into account. It is consequently super- fluous to go again into the details of a combination of insufficience and stenosis, and it will be enough to recall the fact that the aortic valves differ from the auriculo-ventricular, inasmuch as both stenosis and insufficience occur in an isolated condition oftener on the former than on the latter. Further, we should not forget that on an auriculo-ventricular valve, especially on the mitral, one form may gradually overbalance the other during the course of the disease. For instance, a case of mitral insufficience may VOL. VI.—11 162 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. be complicated by stenosis of the orifice, and finally this stenosis may take such possession of the foreground that the main physi- cal symptoms belong more to it than to the insufficience. The simultaneous combination of affections arising on differ- ent valves and orifices, is of special importance, both as regards the modifying influence it exerts on the secondary changes in the heart and the difficulties it adds to the diagnosis. Its occurrence is by no means rare (in about 10 per cent.), and it may arise at the very beginning of the disease, as when a number of valves together are attacked during acute rheumatism. But the more usual case is the gradual spread of the disease from one to another during the course of some already existing valvular or ostial affection. I do not coincide in the view, held by Gerhard and others, that the mechanical condition of tension produced by the affection of one valve tends to injure the other valves ; for were this so, we should see anatomical changes in the tricuspid valve much oftener, apart from relative insufficience, when the mitral has been previously attacked. In cases where, from the beginning, the same harmful influences have not operated simul- taneously on different valves, it is simpler to look for the cause of the anatomical extension of the disease in the contiguity of the parts, particularly as it occurs most frequently on the mitral and aortic valves, where the transition is rendered so easy by the aortic flap of the former, that we can only wonder this combina- tion does not occur still oftener. The modifying influence of a combination of valvular diseases is most plainly exerted on the heart itself by a simultaneous in- sufficience of the aortic valves and stenosis of the mitral orifice, or stenosis of the aortic ostium and insufficience of the mitral valve. In the first case, especially if the disease began on the aortic valves, part of the influence of the stenosis of the mitral orifice is exerted on the left side of the heart, the left ventricle being usually found hypertrophied instead of atrophied. But the degree of dilatation and hypertrophy cannot be so great as when the blood flows unhindered from the left auricle. On the other hand, the secondary dilatation and hypertrophy of the left ventricle may be very considerable in the second case, where there is at the same time stenosis of the aortic valves and insufficience COMBINATION OF VARIOUS VALVULAR AFFECTIONS. 163 of the mitral, for under these conditions the two diseases tend to produce the same effect on this ventricle. The mechanical results of this combination are the most unfortunate, for both hinder the supply of the aortic system. Besides, though the defects of the aortic valves seldom produce any indirect effect on the right side of the heart, still, when combined with mitral deficiency, they may produce a highly beneficial change in the right ventricle. Stenosis of both orifices of the left side work in the same self- correcting manner Avhen they arise at the same time, the results being concentric atrophy of the left ventricle and dilatation and great hypertrophy of the right side of the heart. My own expe- rience, as regards the condition of the left ventricle in a case of in- sufficiency of the aortic and mitral valves combined, does not agree with that of Friedreich and Dusch. These authorities assert that the greatest excentric hypertrophy of the left ventricle is reached in this combination ; whereas I have only observed very great dilatation, without hypertrophy, of the left ventricle, and on the contrary, the right ventricle was so very much dilated and hypertrophied that the apex of the heart even was formed by it. The degree of perfection and the time of development of each factor of the combination exert the main influence on the final result of the whole. Of the simultaneous defects of the valves on both sides of the heart, the most frequently occurring combination is that of steno- sis of the mitral orifice and relative insufficience of the tricuspid valve. Since the latter is evidently a result of the former, it is indeed perhaps unfair to call it a combination. The relative insufficiency, while it lasts, diminishes the tension in the pul- monary artery caused by the stenosis of the left venous ostium, and thus performs a certain amount of compensatory action. Constriction of the ostium venosum dextrum occurring simul- taneously with stenosis of the pulmonary artery, and insuffi- ciency of its semi-lunar valves, is a combination of the rarest occurrence, there being only one case on record. The action of the latter affection modifies the change of volume of the right ventricle. Wherever a combination of valvular diseases exists the phy- sical symptoms are correspondingly manifold, and from the 164 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. signs peculiar to each factor we may construct a scheme of the whole. Thus it is self-evident that, if for instance a systolic blowing sound with maximum intensity over the apex be heard in insufficience of the mitral valve, and if in insufficiency of the aortic valves we perceive a diastolic murmur, with its maximum intensity over the ostium of the aorta and on the sternum, we may expect, when the tAvo affections are combined, to hear both a systolic and a diastolic murmur, with their maximum intensityl each in its respective place. In the same way, for every com- bination we can construct a series of auscultatory and percus- sional signs, which should theoretically be heard. But in reality, things are not so. The combinations are extremely difficult of recognition, far more so than theory would lead one to expect. The reason of this lies in the easy transmission of the murmurs from one ostium to another, thus throwing the whole difficulty of isolating the different affections on the discrimination of the timbre. But even this differentiation deserts us, when, as in a combination of aortic and mitral insufficience, we might be led to expect a pregnant distinction from the whirring character of the one and the blowing character of the other. We must consequently direct all our efforts to find the situation of each murmur's maximum intensity when many are present, and also to distinguish the timbre peculiar to each. If we can succeed in this, it is possible to make a diagnosis of several valvular affections together. This diagnosis is not alone scientifically interesting and indispensably necessary for the comprehension of the separate factors of the case, but it must also be brought well into account in forming the prognosis. For, as is plain from what has been already set forth, the effect of a second on an alread}7- existing valvular disease may, according to the nature of the second, be either very injurious, or at least tem- porarily favorable. Treatment of Valvular Diseases. It is useless to talk of prophylaxis for valvular disease in most cases, for the endocarditic as well as the atheromatous processes TREATMENT OF VALVULAR DISEASES. 165 frequently run such an imperceptibly slow course, that we seldom know of their existence till the circulation begins to be impaired by a disturbance in the function of the cardiac valves and dimi- nution of the vascular elasticity. However, in as far as in youth and middle age rheumatic fever is the undoubted cause of endo- carditis, and as for later years Ave may reckon, among the causes of the atheromatous process, both abuse of alcoholic drinks and immoderate smoking, the avoidance of all harmful influences which have a tendency towards rheumatism or atheroma may be considered at the same time of great prophylactic importance for valvular disease. Special care should be shown in the hy- gienic regulations made for individuals, in whose family heart disease has often been observed, since statistics do not allow us to quite throw aside the doctrine of hereditary predisposition to affections of the heart and vessels. Under such conditions a plrysician should be consulted before a young person chooses his profession. But it is only possible in a few cases to carry out this kind of prophylaxis, as it seldom happens that the phy- sician has opportunity of becoming intimately acquainted for any length of time with the patient and his private affairs. We generally have to face the fait accompli of a fully-developed heart disease. In fact, medical advice is seldom taken till the signs of slight derangement of compensation first attract the attention of the patient himself. For, since nature more or less compensates any derangement of the central circulatory appa- ratus, by a parallel development of dilatation and hypertrophy in the corresponding ventricle, the patient himself remains un- aware (at least under favorable conditions) of any symptoms of his disease. However, quite casual matters, such as over- exertion in taking a very long wlak, or in climbing a mountain, the necessity of performing some arduous work, a slight cold with succeeding catarrh of the respiratory tract, psychical emotion, Avhether of joy or sorrow, any of these, by means of palpitation and dyspnoea thereby developed, may arouse the attention of the patient and physician at a stage when the compensation is still perfectly sufficient for all the circumstances of every-day life. The physician must pursue very different courses, according as he is called in at a stage where the compensation is sufficient for 166 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. ordinary daily life, or when his aid is not sought till signs have set in of severe derangement of the compensation. The first and most fundamental rule which holds good here and in all other chronic diseases, though one that is often neglected, in spite of its self-evident simplicity is, not to make the case worse by the use of drugs. As far as the patient's social position and calling will allow, general hygienic measures should be taken to main- tain as long as possible the natural correction exerted by the development of hypertrophy. The indication we have is, to advance the development of compensation when already in ex- istence, to maintain it as long as possible, and to moderate over-compensation. Accordingly, to promote and preserve the compensation, the diet of the patient should be nourishing but not stimulating. Animal and farinaceous food may be taken according to indiAddual taste. Those vegetables should be avoided which develop much gas, and thus interfere with res- piration. Coffee and tea should only be taken when extremely weak, the form known as family coffee ; spirituous liquors, espe- cially punch, grog, etc., and much smoking, should be equally disallowed. On the other hand, a light bitter beer and a little good wine are to be recommended as aiding the digestion. But the best means for promoting a good digestion are fresh air and exercise. This latter, however, must be taken cautiously, and all severe exertion, such as mountain climbing, etc., should be strictly avoided ; but it is just as injurious to condemn a patient with heart disease to perfect quiet. Where means allow, we should try to procure a few hours daily in the open air, during the winter months as well, and people who can afford it should be sent to some sanitarium like Pau, Pisa, or Mentone. On account of the important part the vessels of the skin play in moderating and regulating the circulation in the internal organs, we should not undervalue the importance of a regular culture of the skin. Lukewarm, plain, or saline baths, with a cold rub- down afterwards, act favorably, by attracting the blood into the peripheral vessels, and by producing a general vigor of the functions through the influence they exert on the sensory cuta- neous nerves. Some time ago great alarm prevailed about over- excitement of vascular activity by too hot baths in heart disease; TREATMENT OF VALVULAR DISEASES. 167 but the extremely favorable results obtained by Beneke in Nauheim in the use of saline baths containing carbonic acid, at temperatures from 88° to 93° F., obtained even in cases of severe derangement of compensation and recorded most accurately. have completely set aside this alarm. Even at the stage where compensation is still almost sufficient, we may modify and combat the unusual irritability of the heart, displayed in the palpitations which occur with the least exertion or even while the patient is at rest. Psychical as well as physical stimulants must be as much as possible removed. Olympian calm, AAdien its attainment is possible, should be warmly recommended as the mental dietary of a heart-disease patient. The patient's attention should never be attracted to his disease either by those about him or by the physician. There are a number of drugs specially suited to allay the pathological irritability of the cardiac muscle, Avhich may be regarded as the first sign of exhaustion in the struggle against the mechanical difficulties. At the head of these stands the application of cold. I have repeatedly seen good results obtained from the old method of allowing patients, troubled with palpitations, but without any symptoms of bad derangement of the compensation, to carry a few hours a day a metal or gutta-percha vessel (adapted to the cardiac region and with the concave surface against the ribs), filled Avith cold AArater or ice. On the other hand, I cannot speak for the use of lasting irritants on the skin (blisters, issues, etc.), so much recommended after the English practice ; indeed I consider them injurious. Of the narcotic agents, preparations of hydrocyanic acid, such as cherry-laurel water or bitter almond-Avater, and tincture of belladonna, act favorably in combination with valerian. But the sovereign remedy, which may be used in every stage of valvular disease with merely variations in the doses, is digitalis. Experience teaches us that a combination of digitalis and iron preparations is specially serviceable in combating abnormal irritation of the heart, and that there need be no apprehension whatever of stimulating the heart's action by moderate use of the iron. I usually prescribe a mixture of two parts each of the tinctures of digi- talis and valerian, and three parts of ethereal tincture of acetate 168 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. of iron.1 Of this I give twenty-five drops three times daily. If no special counter-indications are exhibited, the patient takes this for fourteen days regularly ; but after this it should be given up, except in attacks of palpitations, and then it may be replaced by steel drops alone. For the same object, and es- pecially for longer continuous use, Botkin reccmmends nitrate of silver alone or combined with digitalis. He administers it for five or six weeks in pills of one-sixtieth of a grain three times a day, and, as the activity of the heart increases, he raises the dose every three or four days by one pill of the given composition, till he reaches one-sixth of a grain per diem ; then he diminishes the dose rapidly, but does not leave off the medicine at once. If the irritability be very great, he adds one grain of digitalis to the dose of nitrate of silver. I have had no experience myself of this treatment, but did not wish to pass over the advice of such a tried physician without mention. But as long as it is at all possible, we should hesitate to use any drugs whatsoever, except tonics. Further, Ave should not forget in using digitalis that, on the one hand, its long-continued use acts injuriously on the digestive organs, and that, on the other hand, the medicine is chiefly indicated when it can make the action of the heart more regular by retarding it, and when it can raise the decreasing tension in the aortic system. Slight stagnation, which occurs as the first symptom of a slower circulation in the glandular organs of the abdomen, the trifling swelling of the liver, and its accompanying gastric catarrh, all these require to be counteracted by the use of bitters and gentle aperients, in the shape of saline mineral waters. Favorable results are obtained with rhubarb, in its different preparations, with quassia, gentian, and the waters of Homburg and Kissingen, and especially with the hot springs of Soden. They remove this complaint temporarily, so that the strength of the patient im- proves with renewed appetite. When dropsy occurs, the case is far more difficult to treat. The first warning we get of this, is a swelling around the ankles, which merely makes the patient com- plain that his boots squeeze him in the evening and feel too 1 Solution of acetate of iron, 9 parts; alcohol, 2 parts; acetic ether, 1 pa.it. —German. Ph. TREATMENT OF VALVULAR DISEASES. 169 tight; but this generally disappears with just a little rest. Rest, too, and a horizontal position, are efficacious in more serious cases as Avell, for the swelling does not increase if they are observed ; but to banish it completely, we must use diuretics and stimulants for the intestinal secretion. At the head of these stands acetate of potash, when the pulse is still vigorous and the cardiac action regular. If the digestion is good, I generally combine it Avith iron (acetate of potash, two drachms; ethereal tincture of ace- tate of iron,1 forty-five minims ; raspberry syrup, five drachms ; water, to make six ounces), which has the further advantage of increasing the intestinal activity in addition to its diuretic power. Squill may be reckoned among the tried diuretics, and may be administered as vinegar of squill, with carbonate of potash added to saturation, thus combining the action of both drugs. This medicine, however, cannot be employed if there is any intestinal catarrh, or if it produces any tendency to vomiting, as some- times happens even in cases quite free from catarrh. In such cases Ave can recommend the vegetable diuretics, such as lovage root, rest-harrow root, and juniper berries. I have never seen any great success attained by the use of the diaphoretic methods through internal medicines in dropsy from stagnation. But Avhen the pulse is low, the action of the heart irregular, and the urine scant}', though containing no foreign elements—in a word, in the condition A\-hich Beau has described as "asystole," and which now goes under the name of the " stage of disturbed com- pensation," the diuretic value of digitalis, in small doses, par- ticularly Avhen combined with quinine, is inestimable. At this stage, as Traube's brilliant and thorough researches have taught, there is no better tonic for the cardiac muscle than digitalis, in small doses. After administering nine grains of digitalis, in in- fusion Avith tAvelve of muriate of quinine, I have seen consider- able drops}r, Avith a daily secretion of from five to ten fluid ounces of urine, disappear in a short time, while the urine rose to sixty-eight fluid ounces and more. While the intestinal canal remains intact, we may try to combat the dropsy by the use of drastics, and for this purpose special credit is given to gamboge and See foot-note on preceding page. 170 EOSENSTEIN.—DISEASES OF THE ENDOCARDIUM. scammony. It is, however, better to avoid these methods, with the object of removing every possible abnormal irritation from organs which of themselves are extremely liable to secondary affections. When the oedema steadily increases, in spite of all internal remedies, the only remaining course to get rid of the fluid is scarification. A number of pretty deep incisions a few lines long allow the serum to flow off freely ; then we have only to avoid all erysipelatous inflammation of the skin by keeping the wounds perfectly clean, and this is best effected by bandages steeped in chlorine and chamomile waters. I have seen as great, though not as lasting, success in promo- tion of cardiac and renal activity, from the use of the pneumatic method, lately added to the medicinal repertoire. The observa- tions which I have made on the results of Waldenburg's appa- ratus fully confirm the inventor's expectations, founded on theo- retical grounds. The compressed air, as it is inspired by means of this apparatus, raises the tension of the aortic system. Though Drosdorff and Botschetchkaroff ' found in their physiological ex- periments on dogs that the arterial pressure fell as soon as the animal inspired compressed air, I can, on the contrary, adduce cases of patients whose pulse could scarcely be felt, and most cer- tainly not counted, but after inspiration of compressed air, it grew so full and strong that it could be quite easily counted ; and, fur- ther, the diuresis, which had been extremely scanty, rose consider- ably, though no disturbing influence, in the way of drugs or change of diet, had been employed. On this latter symptom I lay pecu- liar stress, as it is quite independent of any subjective influence. Haenisch's2 researches, too, clearly show that, under the influence of compressed air, the systolic elevation of the ascending limb of the sphygmographic tracing rises higher, and the elevation of recoil on the descending limb is less pronounced. He further shows that the symptoms of a deranged compensation were met by this agent, and corrected. Though I consider myself justified in placing the influence of compressed air parallel to digitalis in small doses for heart disease, yet it must be admitted, that, as 1 Med. Centralblatt, 1875, No. 5. 2 Deutsches Archiv. Bd. XIV. Heft 5 and 6. TREATMENT OF VALVULAR DISEASES. 171 far as a lasting effect is concerned, my oAvn experience convinces me that digitalis, when its continuous use is well borne, is un- doubtedly superior, and this applies also to its regulatory and re- tarding action on the pulse. On the other hand, the pneumatic method must be considered a valuable substitute for digitalis in all cases where this latter cannot be administered on account of gastric complications and generally where it does not agree with the patient. Respiration of compressed air is indicated, as is digitalis, in small doses, in mitral affections, especially stenosis of the ostium venosum sinistrum, and in stenosis of the aortic ostium, when the compensation becomes deranged. In insuffi- cience of the aortic valve, digitalis may be considered as a means of moderating over-compensation, and must then be given in larger doses. I am not able to judge the effect of breathing rarefied air, from personal experience. But on theoretical grounds, it would be indicated in those cases of heart disease where we wish to raise the tension in the lesser circulation. If we succeed (whether by the pneumatic method, or by the use of digitalis) in regulating the pressure relations in the arterial and venous systems, we have overcome in the best possible way the worst subjective troubles, especially the palpi- tations, the feeling of terror, and the dyspnoea. But all these afflictions are, in a whole series of cases, more directly dependent on nervous influences, and often occur in paroxysms, even though the general conditions of the circulation remain un- altered. Pain, too, frequently accompanies these. In such cases a very favorable effect is produced by the subcutaneous in- jection of morphia. I have seen patients who could not lie in bed, and who were consequently much reduced by sleeplessness, living quite comfortably for months with this treatment. But, on the contrary, the greatest caution should be taken in admin- istering chloral to patients with heart disease. It is impossible to form any estimate previously as to the individual powers of sustaining the depressing influence of chloral on the excito- motor ganglion system of the heart. The evidence as yet has not gone to support Liebreich's opinion, that croton-chloral pro- duces better results in heart disease than chloral itself. The secondary affections of the organs and functional disturb- 172 ROSENSTEIN.—DISEASES OF THE ENDOCARDIUM. ances must be treated according to the general rules for these conditions, whether the trouble be in the brain (apoplexy, embo- lism), in the bronchi and lungs (bronchitis, haemoptysis, pneumo- nia, hemorrhagic infarction, threatening pulmonary oedema), in the pleura, or in the kidneys. These are only modified by the primary cause, the valvular disease, in so far that we must always take into consideration that most are produced by the weak condition of the heart. We must specially emphasize the necessity of prompt medical assistance in the treatment of faint ing and dizzy fits, so often exhibited by patients with stenosis of the aortic ostium. Such cases arouse alike the anxiety of the physician and that of the patient's friends. The prompt applica- tion of volatile stimulants (ether, Hoffmann's anodyne, wine) is urgently necessary, and the head should be placed low, while the body lies horizontal. It is not improbable that nitrite of amyl, administered cautiously (five drops for inhalation), would produce a favorable result. On the other hand, the venous stases of the brain, which exercise a certain influence on the mental action, in defects of the auriculo-ventricular valves, or the active congestion which occurs in insufficience of the aortic valves, must be com- bated by fontanelles, sinapisms, or dry-cupping on the neck, or else by small local bleedings over the mastoid process. In treat- ing haemoptysis, arising from an affection of the left venous ostium, we should not forget that when the bleeding is not suffi- cient to compel active measures, it relieves the lesser circulation of a superfluous load, and thus produces a beneficial effect on the general condition of the patient and his dyspnoea. « / V CHANGES IN THE POSITION OF THE HEART DISEASES OF THE HEART STJBSTAICE. SCHROETTER. CHANGES IN THE POSITION OF THE HEART. The manuals and handbooks of Laennec, Andral, Cruveilhier, Rokitansky, Fdrster, Bock, Bamberger, Lebert, Trousseau, Duchek, Klebs, Dusch, Jaccoud and others.—i Gilbert Breschet, Mem. sur l'ectopie du cceur. Paris, 1826.—Karl Ewald Hasse, Anatom. Beschreibung der Krankheiten der Circulations- und Respirations- organe. Leipzig, 1841.—J. Engel, Darstellung der Leichenuntersuchungen und deren Bedeutung. Wien, 1854.-- William Stokes, The diseases of the heart and aorta.—Da Costa, Effect of respiration on the size of the heart. Americ. Journ. of Medical Science, Oct. 1859.—Bamberger, Ueber die Lage des Herzens beim Lungenemphysem. Wurzburger med. Zeitschr. I., 419, 1860.— TU. Kobelt, Ueber Form und Dimension der Herzdampfung. Inaugural-Dissertat. Giessen, 1863.—Engel, Ueber einige pathol. anatom. Verhaltnisse des Herzens. Wiener med. Wochenschrift, 44, 45, 46, 1863.— W. C. Maclean, Report of a case of lateral transportation of the heart and liver in a soldier. Lancet, 8. Aug. 1863. —Gerhardt, Ueber einige Formen der Herzdampfung. Prag. Vierteljahrschr. IV. S. 113, 1864.— E. Rindjleisch, Ueber eine eigenthiimliche Drehung des Fliissigkeitsstromes im elastischen Rohre, iiber die Lageveriinderung des Herzens und den Situs viscerum per versus. Hermann's med. Centralblatt, No. 21, S. 323, 324, 1864.—Greenhow, Displacement of the heart to the right side, con- sequent upon disease in the right lung. Transact. Path. Soc. XIX. p. 159, 1869.—Schrbtter, Beitrag zur Kenntniss der Lageveranderungen des Herzens. Oesterr. med. Jahrb. XX. S. 189, 1870.—E. Rindjleisch, Lehrbuch der patholog. Gewebelehre. 3. Auflage. Leipzig. Seite 198, 1873. The changes in the position of the heart form no independent disease, but are only the indication of pathological alterations, less frequently in the heart itself than in adjacent organs. But since the determination of the position of the heart is of great importance in coming to accurate conclusions as to the condi- tion, not only of the thoracic viscera, but frequently of the entire system, it seems quite proper to devote an independent chapter to this subject. If Ave reject congenital anomalies, such as transverse position 176 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. of the heart, abnormal origin of vessels, etc., the changes in posi- tion may be classified as follows : 1. Turning of the organ on its axes. 2. Change in position, according to the laws of gravitation. 3. Pressure of the heart to right or left—upward or down- ward. 4. Traction on the heart producing same effects. Before beginning, it seems best to describe the normal posi- tion of the heart. Normal Position of the Heart. As the heart rests on the anterior portion of the central ten- don of the diaphragm, the position of the organ is such that its long axis forms an angle of 60° with that of the body, and the portion which is lowest and furthest removed to the left is the apex of the organ. Inasmuch as the apex is the part whose lo- cation can best be established, it is of great importance in deter- mining the position of the heart; if Ave succeed in exactly locat- ing its beat, we can give the position of the whole heart with considerable accuracy. In by far the greatest number of healthy individuals, the apex is found in the fifth intercostal space, about a thumb's breadth inside the left nipple. Not unfrequently it lies in the fourth intercostal space, and then usually close to the nipple, occasionally in the sixth ; but so rarely does this occur with the healthy organ, that under these circumstances we are justified in suspecting pathological changes ; but we must remember that in little children the apex is very frequently found in the fourth intercostal space, and in old people in the sixth. To this extent age has an influence on the position of the heart, namely, in so far as it affects the position of the diaphragm. In childhood this depends, doubtless, on the more active contractile power of the lung. Beside these, we must remember that in the gradual de- velopment of the system the aorta grows longer, and so the heart comes to lie lower in the thorax. Towards the right, the heart extends about three fingers' breadths beyond the median line, and the parts found here are the right auricle and a small por- TURNING OF THE HEART ON ITS AXES. 177 tion of the right ventricle, in front, and, deeper in, the right half of the left auricle as well. The anterior surface is largely covered in by the edges of the lungs, so that only a small portion of the right ventricle, which generally makes up the greater part of the anterior surface, lies in contact with the chest-wall. As regards inspiration, we must remember two points : First.—The heart descends with the descending diaphragm, and frequently to the extent of a whole intercostal space. Secondly.—The lung presses further and further forward over the heart, and in deepest inspirations it expands until arrested by the reflection of the pleura costalis on to the lung, on the one hand, or, on the other, by the connection of the fibrous pericardium with the chest-wall, by means of the so called liga- menta sterno-cardiaca superius and inferius. In the most extreme expansion of the lung there remains uncovered only a small triangular portion of the anterior surface of the heart, which lies at the lower end of the sternum, extend- ing from the median line towards the left. For aid in physical diagnosis we must consider, that if we make a longitudinal section (as Luschka has done) through the median line of a frozen body, we find in the right half the right auricle, the right half of the left auricle, a small portion of the right ventricle, and only a very small portion of the septum ven- triculorum ; while in the left half of the body we find the left half of the left auricle, the Avhole left ventricle, by far the greatest portion of the right ventricle, with the greater part of the sep- tum ventriculorum. As regards the upper limit of the heart, the highest portion is the top of the left auricle, which reaches as far as a horizontal line, which, if produced forward, touches the lower border of the second costal cartilage. Turning: of the Heart on its Axes. Turning of the heart on its long axis generally occurs in such a manner that the right auricle and ventricle come to look more directly forwards, and the left cavities backwards. Such changes are quite rare, especially when existing alone, and usually are occasioned by simultaneous dislocations of the heart, arising VOL. VI.—12 178 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. from antecedent pressure, or from traction upon the organ by the contraction of adhesions in the pleura, or more rarely by contracting bands in the lung itself. Bamberger relates a case of pneumo-thorax on the left side, in which the heart was not only pushed over to the right, as is usual, but had so reA^olved on its long axis that the greater por- tion of the left ventricle looked forward ; this revolution was so considerable that torsion of both the great vessels could be easily recognized. It is hard to picture to one's self how this came to pass, inasmuch as there were no contracting bands found here, and it may be that, with an original tendency of the heart in that direction, a weak spot in its suspension gave occasion to the displacement and torsion. Revolutions on an antero-posterior horizontal axis occur especially in cases of aneurism of the ascending aorta, when extension of the aneurism downwards presses the base of the heart down, and the apex rises. This same axis-revolution occurs in other cases of pressure, which will be mentioned here- after ; but, in comparison with the changes in position which the heart undergoes at the same time, it is of minor importance. Changes in the Heart's Position dependent npon Gravitation. In spite of opposing statements, it is now settled beyond all doubt that, in changes of position of the body, the heart follows the laws of gravitation. The displacement towards the left, where the impulse is dis- tinctly to be felt, is by far the most noticeable ; that towards the right is only slight. Doubtless, when the body is bent forwards, the heart lies in contact with the anterior chest-Avail over a greater extent, as is learned by careful percussion. Adhesions which the pericardium alone or the heart and pericardium have formed with the neighboring parts will limit the mobility of the heart as decidedly as stronger indurations and immobility in adjoining organs which cannot yield to the pressure of the heart. A considerably hypertrophied and dilated heart, as Avell as one suffering from new-growths, will by its weight press the dia- phragm downwards ; this displacement is, however, by no means CHANGES DEPENDENT UPON GRAVITATION. 179 so great as occurs occasionally from the same cause in pericardial effusion; if this is so great as to be found, not only at the base, but also on both sides of the heart, the depression of the arch of the diaphragm will be still more marked. What position does the heart take in vesicular emphysema of the lungs ? It follows the law of gravitation here, for, as it rests upon the diaphragm, when this is depressed, in consequence of extreme expansion of the lung, the heart descends as well; the question is, what position does it assume in this case. Upon this point there are tAvo opposing views. The older, maintained especially by Skoda, holds that the heart presses downwards with its apex, and the organ, as a whole, is brought nearer to the median line. Bamberger, on the other hand, claimed that, as the base was pressed down, the heart assumed a more horizontal position. The grounds upon which Skoda based his view were: the recognition of the impulse of the heart, not at its proper site, but nearer the median line, even in the scrobiculum cordis (often with such distinctness that you can feel a pointed object thrusting itself between the finger-tips applied to the chest); also, in part, the harmony of this view with the results of autopsies ; and, finally, the probability that, in the depression of the heart, the apex, which is the most movable portion of the organ, would be affected rather than the base, which is the least movable part. Bamberger, on the other hand, held that that which we feel beating in the scrobiculum cordis is not the apex, but a portion of the wall of the right ventricle, inasmuch as, by seeking carefully, we can find the apex beat in its normal place, and, moreover, in autopsies the heart has been found lying horizontally. Concerning this last point, Prof. Klob has given us some valuable information, by shoAving that we were not authorized in thinking that the heart necessarily had the same position in life as in the cadaver. The rigor mortis, the distention of the intestines with gas, and other causes, must naturally alter the position of the heart after death, and it is only by fixing the heart in situ with needles passed through the chest-wall, as soon as possible after death, that we can be sure of its position during life. I have followed up this subject with some care, and have 180 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. arrived at the following conclusion. In the more advanced stages of emphysema the apex lies considerably further to the right than normal, but certainly that which we feel giving the impulse in the scrobiculum cordis is not always the apex, as this frequently lies directly behind the point of junction of the left costal cartilage with the sternum, but is actually a portion of the wall of the right ventricle. In the recumbent position we cannot, after the most careful search, find the apex beat at its normal place ; but if we cause the patient to turn towards the left, we can very frequently find the apex between the left edge of the sternum and its normal site, more or less near to the latter, and in this way we learn that the heart, displaced by disease towards the median line, is now by a change in position caused to fall towards its normal place. Now, if we observe an extension of the heart dulness beyond the right edge of the sternum, while it is but slight towards the left, this is occasioned by a change in the position of the heart, and not by hypertrophy of the right ventricle, for hypertrophy of this ventricle to any great extent is by no means the rule in all cases of emphysema of the lungs ; nor is it always found in post-mortem examination ; but in this case the epigastric pulsa- tion may have been very forcible, yet, on the other hand, you will find that in many cases of advanced hypertrophy of the right ventricle no epigastric pulsation is observed. Accordingly, though I accept it as a rule that the apex presses downwards towards the median line, I cannot deny that several cases of ex- tensive emphysema have been observed by me where the dulness over the heart was limited in extent (by encroachment of the lung), but the apex could be distinctly made out by percussion at its normal place, or even further to the left. These cases would seem to support Bamberger's view, but they are only exceptions, and seem to depend upon some peculiarity of the in- dividual ; for if originally, in a given individual, the heart has a more horizontal position than normal, where the diaphragm is depressed, it cannot press downwards with its apex, but with its base, and thus the heart comes to hold a more horizontal position still. In this manner it seems to me we must explain the rela- tion of the parts in emphysema of the lungs. CHANGE OF POSITION BY PRESSURE. 181 Change of Position by Pressure. The heart is exposed to the greatest pressure in cases of pleuritic exudation and pneumo-thorax, especially of the left side. In cases of displacement towards the left, as the heart rests upon the arch of the diaphragm (and this latter in these cases is always pressed downwards), the apex beat may be seen in the sixth or even the seventh intercostal space in the axillary line. In cases of pressure towards the right we may easily make a mistake as to the cause of the change in position. We must remember that the heart will be pressed over to the right in the same relative position as in health, and accordingly cannot assume a position such as we should find in congenital trans- verse position of the heart. Hence, the apex comes to lie behind the sternum, the xiphoid process, or that cartilaginous plate formed by the union of the costal cartilages of some of the lower ribs; its impulse is, therefore, not felt, and a portion of the right ventricle, lying against the thoracic wall, simulates, by its pulsation, the apex beat. This was most beautifully marked in the person of a student of medicine with intense pneumo-thorax of the left side. Here the impulse of the right ventricle in the fourth intercostal space, about two inches beyond the right edge of the sternum, was so distinct that you would be led to doubt the truth of the above rule; but in this case the usual relative positions of the organs existed ; for, after following the example of Hope and Gendrin, I had fixed the heart in situ by piercing it with needles from without immediately after death, I was able to show at the autopsy how the heart lay just as I have stated above, with its base furthest over to the right, and the apex behind the right edge of the sternum. In pleuritic effusion on the right side we occasionally find a peculiar form of displacement of the heart. If the quantity of fluid is very great, the right lobe of the liver is pressed down- wards and the left tilted up, and the heart by this means assumes a horizontal position, or may even be pressed upwards the breadth of the two intercostal spaces. Pneumonia of itself cannot cause pressure on the heart, for the shrinkage of healthy portions of the lung counterbalances the swelling of the parts affected by the inflammatory process. Occasionally, hoAvever, the heart assumes an abnormal position 182 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. in consequence of a change in the position of the diaphragm ; for if the lung of one side is hepatized throughout, its weight is so increased thereby that it presses upon the diaphragm, which descends, and with it the heart also. I was able distinctly to recognize this change in the case of a young man of 19 years of age with pneumonia on the right side, where the hepatization was so intense that it was mistaken for a pleuritic exudation,—and to confirm my diag- nosis by an autopsy. Smith reports a similar case in the " Dublin Journal of Medi- cal Sciences." Vol. XIX. p. 122. In a pneumonia of this kind upon the left side the changes in position of the heart must be more considerable, but I do not recall any such case. Diseases of the mediastinum in advanced stages influence the position of the heart—such are abscesses, neoplasms, and espe- cially carcinoma ; but these are comparatively rare. Aneurisms of the great vessels, and particularly of the aorta, are of much more importance. If an aneurism has developed in the course of the ascending aorta with dilatation of the vessel and bulging towards the right, generally the heart lies in a horizontal position, and, in advanced stages, suffers pressure downwards and towards the left. Skoda has also seen cases when the heart had partially revolved on its antero-posterior horizontal axis, where the base was pressed downwards and the apex upwards. When the aneurism develops with bulging towards the left, or in the concave portion of the arch of the aorta, the heart will be pushed downwards and at the same time more towards the right. The same is true in cases of aneurism of the pulmonary artery. Curvatures of the spine, when considerable, likewise occasion alterations in the position of the heart. This is particularly true in kypho-scoliosis. From the influence which the position of the diaphragm exer- cises upon that of the heart, it naturally follows that certain abdominal diseases, with the change they occasion in the dia- phragm, affect the heart's position as well. General enlargement of the abdominal cavity, as occurs in ascites, will not alter the position of the heart so long as the abdominal walls yield to the pressure; but when this limit is passed, the diaphragm will be impeded in its descent, will be pressed upwards, and with it the CHANGES DUE TO TRACTION. 183 heart will be pushed upAvards and towards the left; often in such cases the apex beat may be found in the third intercostal space. Abdominal tumors will only cause pressure on the diaphragm, and thus affect the heart, when they are so firmly attached that they can only increase in an upward direction. Diaphragmatic hernia is usually congenital, and, in conse- quence of the non-viability of the children, does not come partic- ularly under our observation. Occasional instances, however, may be found in the literature of the subject: Weiland in Bouillaud.—In a case of diaphragmatic hernia, the left half of the thorax was found filled with coils of intestine as high as the second rib, and the heart was thereby pressed over towards the median line; the child lived seven years. Skoda recalls an autopsy on a man who died at the age of forty of tuberculo- sis, where he found the heart pressed over to the right by the stomach and portions of the transverse colon which lay in the left thoracic cavity. In " Cruveilhier's Pathological Anatomy" we find the case of a woman of seventy-five years of age in whom the heart was found lying entirely in the right side, being pressed over by a diaphragmatic hernia. Sennert (Practica P. II, P. 2, chap. 15, p. 703) relates the case of a student who died suddenly eight months after receiving a dagger wound in the breast, which had entirely healed, and it was found on examination that the diaphragm had been perforated and the stomach lay in the left thoracic cavity, pushing the heart over towards the right side. Changes in Position occasioned by Traction. The changes in position Avhich the heart undergoes, in conse- quence of traction by neighboring organs, are very interesting. As regards the lung, we must remember that in consequence Of its innate power of contraction, and continuous attempts to accomplish it, in all cases where one-half of the thorax is filled with pathological products, the heart is drawn over to the healthy side. This holds especially in pleuritic exudations, partial em- physema, and pneumo-thorax ; but in these diseases only to a moderate extent. It is different, however, when, as a result of contracting induration, there is a diminution in the size of the lung. In these cases the change of position in the heart is often very great. I have had under observation for the last seven years a young girl, now eighteen years of age, in whom, as a result of chronic pneumonia, following measles, with 184 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. subsequent contraction of the lung and bronchiectasis, the heart is drawn so far over to the left and upward, that the apex beat is found in the axillary line at the third intercostal space. Several years since I described the position of the thoracic viscera in a man in whom, doubtless from the same cause, the heart was found in the right axillary region. In this case, if we wish to explain it thoroughly, we must assume that behind the contraction of lung as a cause there lay a congenital dex- trocardia. A contracting pleuritic exudation occasions the same changes in the position of the heart. Tumors of the abdominal cavity, if they have reached a con- siderable weight, and are attached to the diaphragm, may pull it downwards, and with it the heart. It is particularly tumors of the liver, and more rarely of the spleen, which are able thus to overcome the contractile power of the lung. Diminution in the size of the liver and spleen, and indeed of the abdominal viscera, generally occasions no change in the posi- tion of the diaphragm and the heart, for in these cases the abdominal walls alone sink in. Pathology. Course of the Disease. The change in the position of the heart as such, as a rule, occasions no functional disturbance. The more extreme displace- ments, however, may, from interfering with the normal contrac- tile power of the heart, or insufficient filling of its cavities, give rise to a tendency to stasis and its results. This will depend chiefly upon the condition of the heart as regards its nutrition and functional power. So likewise the circulation will suffer when the great vessels have been twisted or bent. In such cases murmurs may be developed over the great vessels which simulate lesions of the valves. In a case of very extensive pleuritic exudation, in which the heart was pressed very far over to the left and downwards, in listening over the heart, I heard a loud systolic murmur. The autopsy revealed no alteration whatever in the valves, and I believe the murmur was occasioned only by the stretching of the aorta. 1 Jahrbuch der k. k. Gesellschaft der Aertze, in Wien. V. u. VL Heft. 1870. PATHOLOGY.—COURSE AND DIAGNOSIS. 185 Forster states that interference with the circulation will give rise to hypertrophy of the heart. Frequently special nerve symptoms are associated with it. In a patient in whom the heart had been pushed over into the right thoracic cavity, as the result of a wound, for years after, the heart still remaining dislocated, any excess in eating would bring on vomiting, pain, and a sense of tension or tear- ing in the right breast. In this case, however, we must remember that the pleura had been wounded, and doubtless the ramifications of the vagus came to lie in abnormal positions. Besides this, there was a very singular disorder of sensation. Application of cold in the region of the right breast would occasion attacks of suffocation; dipping the right arm in cold water, besides giving rise to peculiar feelings in the right breast, would cause cramp-like contractions of the right arm, drawing it over towards the breast. Palpitation of the heart, which is frequently observed in con- nection with curvature of the spine, depends not only upon change in the position of the heart, but also upon simultaneous interference with the circulation in other ways. Diagnosis. If we can feel the impulse of the heart distinctly, the diag- nosis of a dislocation will present no particular difficulty, and only at the first glance could we mistake it for an aneurism. The next point is to find the cause of the dislocation. This also, as a rule, will not be hard to discover, except when the signs are obscure and apparently contradictory, as, for instance, in the case mentioned above of diaphragmatic hernia observed by Stokes, in double pneumo-thorax, and others. If the heart's impulse is not distinctly to be felt, then the case is quite different. Here we must try if changing the patient's position to right or left may not make it perceptible. Occasionally we may find it by putting the patient in a stooping position ; let him stand and bend for- ward, resting his hands on the edge of a bed or a chair. If these means do not accomplish the purpose, then we must fall back upon the fact that we cannot find it at its normal place, and to that add the results of percussion and auscultation. In regard to percussion, the place and shape of the dulness over the heart are different from that which we find under the 186 SCHROETTER.—CHANGES IN THE POSITION OF THE HEART. head of hypertrophy, and its boundaries can only be made out when the heart is surrounded by air-containing organs. There occur occasionally very peculiar combinations ; for instance, in a case of double pneumo-thorax I could make out absolutely no heart dulness anywhere. In the case of the young girl mentioned above, with dislocation towards the left, over the normal heart region, from the left sternal border over to the mammillary line, the percussion note is perfectly clear, and it is only at the lat- ter line that there begins an irregular dulness, which extends over to the axillary line. Resting upon the evidence of auscul- tation, we must believe that the apex lies where we hear the heart sounds Avith greatest distinctness, and starting from here as one end of the long axis, we locate the base by the accentua- tion of the second sound in the pulmonary artery. It is clear enough, from what has been said above, that there are often many difficulties to overcome, even with this assistance. In complicated cases we shall have to call in every aid, such as the history of the case, etc., to assist us in forming an accurate diagnosis. Prognosis and Treatment. Both these will largely depend on the underlying cause of the displacement, inasmuch as the heart itself rarely suffers. Some heart symptoms will, however, be considered further on, in accordance with principles to be there laid down. DISEASES OF THE HEART SUBSTANCE. Hypertrophy and Dilatation of the Heart. In addition to the recognized works on diseases of the heart, consult: Clendinning, London Med. Gaz. 1838.—Bizot, Recherches sur le cceur et le systeme arteriel chez 1'homme. (Memoires de la soc. med. d'obs. de Paris, 1838).— Vernois, Dimensions du cceur chez l'enfant nouveau-ne. Paris, 1840.—Peacock, Monthly Journ. Sept. Oct. Nov. 1854.—Forget, Herzkrankheiten, iibersetzt von AVolf. Giessen, 1855.—Traube, Ueber d. Zusammenh. zwischen Herz-und Nierenkrank- heiten. Berlin, 1856.—Bamberger, Ueber die Beziehungen zwischen Morb. Brightii u. Herzkrankheiten. Virch. Arch. Bd. XI. 1857.—Rosenstein, Beitrag zum Zusammenhange zwischen Herz- u. Nierenkrankheiten. Virch. Arch. Bd. XII. 1857.—C. Gerhardt, Untersuchungen fiber die Herzdimqjfung u. s. w. Archiv f. phys. Heilkunde, 1858.—van der Byl, Med. Times and Gazette. May, 1858.—Filaudeau, Des causes de Thypertr. dueceur. These, Paris, 1858.—Larchcr, Arch, gener. de M6d. Mars, 1859.—Traube, Fall von Nierenschrumpfung mit Hypertr. d. 1. Ventr. Deutsche Klinik, No. 49, 1859.—Gerhardt, Der Stand des Tubingen, 1860.— Wilh. Baur, Ueber reine Hypertr. des Herzens ohne Klappen- Diaphragma. fehler. Diss. Inaug.Giessen, I860.—Liebermeister, Deutsche Klinik, 1860.—Campana, Considerations nouvelles sur l'origine de l'hypertr. et de la dila- tation du cceur. Gaz. des hopit., No. 61.—Duchek, Ueber Hypertr. des Herzens. Med. Jahrb. 1, 1861.—Geigel, Ergebnisse aus 84 Sectionen. Wiirzburg. med. Zeitschr. II. 4. 1861.— Valentin, De l'acetate de plomb dans les hypertr. commen- cantes du cceur. L'union med. No. 110, 1861.—Albert Eulenburg, Ueber den Einfluss der Herzhypertr. und Erkr. der Nierenarterien auf das Zustandekommen von Haemonhagia cerebr. Virch. Arch. Bd. XXIV. 329, 1862.—Erichsen, Zusammenhang von Herz- und Nierenkrankheiten. Petersburg, med. Zeitschr. III. 1862.—Ackermann, Die Wirkungen des Brechweinsteins auf d. r. Herz Virch. Arch. Bd. XXV. 1862.—Scheiber, Zur Lehre vom Herzstosse. Virch. Arch. Bd. XXIV. 1862.—Stark, Vergrosserung des Herzens bei Chlorosis. Arch, der Heilk. 4. Jahrg. S 47, 1863.—Forster, Ueber den Zusammenhang von Herz- und Nierenkrankheiten. Wiirzburg. med. Zeitschr. Bd. IV. 1863.—Skoda, Allg. Wien. med. Zeit. 1863 u. 1864.—Tungel, Einige Falle von Hypertr. des. 1. Ventr. in Folge von Nierenschrumpfung. Klin. Mitth. Hamb. 1863.—Roth, Zum Zusammenhange zwischen Herz- und Nierenkrankheit. Wiirzburg. med. Zeitschr. V. 1864.—Hamernik, Die Grundziige der Physiologie und Path. des. 188 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. Herzbeutels. Prag, 1864.—Lower, Nierenschrumpfung mit Hypert. u. Dilat. des 1. Ventr. Berl. klin. Wochenschr. 1864. No. 37. — Gerhardt, Ueber einige Formen der Herzdampfung. Prager Vierteljahrschrift. Bd. IV. 1864.—F. A. Zenker, Ueber die Veranderungen der willkurl. Muskeln im Typh. abdom. Leipzig, 1864.—Polotebnow, Berl. klin. Wochenschr. 1865. No. 35.—Gouraud, De l'influence pathogenique des maladies pulmonaires sur le cceur droit. These, Paris, 1865.—Rosenstein, Zur Beziehung von Herz-und Nierenkrankheiten. Ber- liner klin. Wochenschr. 1865. No. 4.—Gordon, Case of hypertr. of the heart from renal disease. Dublin Journ. of Medic. 1866.—Liagre, Hypertr. du cceur. Hydropericarditis. Presse med. de Beige, No. 27, 1866.—Da Costa, Med. Memoir of the U. S. Sanitary Commission, 1867.—Maclean, Brit. Med. Journ. Febr. 1867.—Thurn, Wien. med. Wochenschr. 1868. No. 45.—Crocq, Presse med. beige, 21. Jahrg. No. 3. Seance de la Soc. anatom. Bruxell. (Hypertr. d. r. Ventr). 1869.— Wilson Fox, Cyanosis, hypertr. of the heart, chiefly affecting the right ventr. Transact. Path. Soc. XIX. p. 104. 1869.—Skoda, Bemerkungen fiber die Hypertr. des Herz. Klin. Vortrag. Allg. Wiener med. Zeit. Nos. 28, 29, 31, 1870.— Oscar Weitling, Ueber d. Hyp. des 1. Ventr. nach Nierenschrumpf- ung. Diss. Berl. 1870.—Bruzelius u. Blix, Hygiea, 1870.—Axel Key, Nordisk med. Arkiv. Bd. 1.1870.—Myers, London, 1870, Concerning strain of the heart. ■—Thompson, St. Georg. Hosp. Report. Vol. V. 1870.—Da Costa, The American Journ. of the Med. Scienc. for Jan. 1871.—Thomas Clifford Albutt, St.George's Hospit. Report. Vol. V. 1870.—Black, Lancet, 1872, Aug. 24.—Treadwell, Bost. Med. and Surg. Journ. 1872.—Moinet, A treatise of the causes of heart disease. Edinb. 1872.—Traube, Berlin, klin. Woch. 1871. No. 29, 1872. 18 u. 19.— Seitz, Zur Lehre der Ueberanstrengung des Herz. Arch, fur kl. Medic. Bd. XI. u. XII. 1873-1874.-0. Frdntzel, Ueber d. Entsteh. von Hypertr. und Dilatat. der Herzventr. durch Kriegsstrap. Virch. Arch. Bd. 57. S. 215.—C. Handjield Jones, Cases of heart disease affording evidence respecting the action of digitalis. Med. Times and Gazette, Oct. 18, 25, 1873. —Hayden, Hypertr. and granul. degeneration of the heart, acute pericarditis, calcareous transformation of the aortic valves and atheroma of the aorta. Med. Press and Circ. Apr. 2, 1873 History. Under the name of heart disease the ancients comprehended all possible diseases of that organ, and very frequently it signi- fied hypertrophy and dilatation. In later times, also, they con- founded under the general name, induration of the heart, not only the diseases under consideration, but inflammatory dis- orders and neoplasms. Senac is the first to make anjr accurate and definite reference to the condition of the walls of the heart and dilatation of its cavities ; he describes, also, the bulging of HISTORICAL SKETCH. 189 the thoracic wall, occasioned by enlargement of the heart. It is interesting to observe that H. F. Albertini (aa-Iio was born at Bologna as early as 1672) called attention to the fact that the left ventricle was especially prone to hypertrophy, and the right to dilatation. We first find the basis for a thorough comprehension of hy- pertrophy and dilatation mentioned by Lancisi.' He stated the belief that these conditions were frequently the occasion of sud- den death, and described a series of symptoms, such as palpi- tation, difficulty in respiration, etc., which accompanied them. He recognized also, with wonderful clearness, that the cause of hypertrophy lay in various hindrances to the greater and lesser circulations. He had no knowledge, however, of the fact that inflammation might be the occasion of dilatation. He indicated the turgescence of the veins of the neck as a characteristic of hy- pertrophy of the right ventricle, although he was not able to distinguish between secondary symptoms and the primary dis- order. Corvisart retained the name, aneurism of the heart, which he seems to have found in Auenbrugger, and distinguished between active and passive aneurism. He described more thoroughly the mechanical causes of the disease, and is generally considered as the founder of this theory. Laennec and Bertin speak of hypertrophy of the heart, and make the distinction between it and dilatation. Bertin also describes accurately con- centric hypertrophy. It is astonishing that Laennec does not go more fully into the causes of hypertrophy. The literature of that period is filled with the controversies of different AAoiters (Burns, Hope, Williams, and others) concerning the causes of hypertrophy. Bizot,2 by means of his accurate measurements, first laid the foundation for rational comparisons of size and volume. Since the days of Rokitansky and Skoda, both con- ditions have held a more secondary position. But now again, quite recently, through the labors of Peacock, Thurn, Myers, and Seitz, great stress has been laid upon the independent de- velopment of the disease. 1 De motu cordis et aneurismatibus. Romse, 1728. ! Memoire de la Soc. med. d'observ. 1836. 190 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. Introduction. By hypertrophy of the heart we understand an increase in the mass of the muscular tissue, usually associated with an in- crease in volume ; by dilatation we understand an expansion of the cavities of the organ. It seems best to consider the two conditions together, for they are so frequently associated that a separate consideration would involve continual repetitions. These particular forms of heart disease are made especially interesting at the present time, from the fact that so many writers in all directions are endeavoring to show that many cases, not only of hypertrophy, but of dilatation as well, deserve to be considered primary rather than secondary disorders. Both conditions may affect the whole heart, but are usually confined to some one portion ; in accordance with this fact, we distinguish between general and partial hypertrophies and dila- tations, where the diseased condition affects one section of the heart, or perhaps is limited to a single portion of that section, as, for example, hypertrophy of a single papillary muscle, dila- tation of the conus arteriosus in the right ventricle, etc. Under the head of hypertrophy we distinguish the following: 1. Simple hypertrophy.—Increase of the heart in volume, with normal cavities. 2. Concentric hypertrophy.—Thickening of the walls, with diminution in the size of the cavities. 3. Excentric hypertrophy.—Increase in muscular tissue, with enlargement of cavities. Dilatation of the heart may likewise be embraced under three heads. 1. Simple dilatation.—Enlargement of the cavities, with nor- mal thickness of the walls. 2. Active dilatation.—Enlargement of the cavities of the heart, with increase in thickness of the walls ; but since a dila- tation of the cavities cannot be accompanied by a normal thick- ness of the walls except they are hypertrophied, the condition is similar to simple dilatation, which also is the same thing as an excentric hypertrophy. Lastly, HYPERTROPHY AND DILATATION. 191 3. Passive dilatation.—Enlargement of the cavities, with thinning of their walls. Further on we will show how, among the various forms of disease, only excentric hypertrophy and passive dilatation par- ticularly interest us. The first is by far the most frequently observed combination of dilatation of the cavities with hyper- trophy of the walls. The existence of concentric hypertrophy is Avidely denied; and, in truth, proof of its existence is no easy matter, for, in a given case of thickened walls with diminished cavities, the distinction between a heart simply found at its maximum of contraction, and one where there is an actual in- crease in muscular tissue, is very difficult and requires great ex- perience. Nevertheless, we must maintain that there is such a disease, even though it occurs rarely, inasmuch as during life Ave can recognize changes in the pulse, which may be perfectly well explained on the hypothesis of a concentric hypertrophy. By spurious hypertrophy, we understand increase in the in- terstitial connective tissue, of which we shall speak later. Etiology. Hypertrophy always occurs wherever a portion of the heart has been called on to perform work beyond its normal capacity, either to overcome mechanical obstacles or in consequence of increased innervation. Left ventricle.—This is in general more inclined to hyper- trophy than the right, for since it is originally the more power- ful, it will be easier for it to meet any obstacle with increased energy than for the feebler right ventricle, which will sooner yield to such opposition, and hence dilate. In consequence of the innate power in the heart to regulate its own action, all those conditions which interfere in a mechanical way with the emp- tying of the left ventricle, must lead to an increased activity on its part, provided the heart substance is healthy. Such con- ditions are : 1. A narrowing of the aortic opening. It is clear that the nar- rower the opening is, the greater will be the obstruction to the column of blood ; the same will be the case, 192 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. 2. When the aorta is contracted in its ascending portion, or throughout its whole course, or only at the isthmus, where it sometimes becomes totally obliterated, close to the ductus arte- riosus Botalli; these various conditions are almost always con- genital ; the first allusion to such a hypertrophy in congenital narrowing of the ascending aorta is made by J. F. Meckel, in Virchow.1 3. In this connection belongs the diminution in calibre throughout the whole arterial system, as it is found, according to Rokitansky, most frequently in the female sex, and asso- ciated Avith slight development of the sexual organs. 4. The cutting-off of whole portions or regions of the capil- lary system ought to occasion hypertrophy of the left ventricle, and although this is found to be the case for the capillary system supplied by the right ventricle, no such state of affairs is devel- oped in the capillary system belonging to the left heart. For example, after amputation of the thigh, when the capillary system is immensely reduced, there is, nevertheless, no hyper- trophy of the left ventricle. Under this head we must consider the hypertrophy which, as is well known, is a very common accompaniment of Blight's disease. Traube has suggested the very clever theory that it arises from the cutting-off of a certain portion of the capillary system in the kidney, in consequence of which the blood-pressure in the arterial system must increase considerably, and which is further augmented by interference with the escape of fluid from the renal arteries and consequent tendency to stasis in these vessels. Numerous as the contributions are in support of this theory, we have an equal number of proofs that it is untenable. Amongst these we may mention : a, The observation that we find cardiac hypertrophy already developed in that stage of the disease where as yet there is no granular atrophy (and only this condition will occasion capillary atrophy); if Dusch thinks to explain this by saying that at this stage of the disease there is amyloid degener- 1 Virchow, Ueber die Chlorose, Berlin, 1872. S. 10. In the collection at Halle, there is a colossal heart, which in the cadaver occupied nearly all the left half of the thorax, and a very narrow aorta, the cross-section of which is half as small again as that of the pul- monary artery. HYPERTROPHY AND DILATATION. 193 ation, in Avhich no hypertrophy occurs as an accompaniment, we would reply that Ave frequently find absence of hypertrophy Avhere there is even no amyloid degeneration ; b, That after the extirpation of one kidney (Rosenstein'), and the removal thereby of a whole capillary region, there followed no increase of pressure in the aortic system. Beckman,2 on the other hand, produced hypertrophy of the heart by ligation of the ureter in a dog. From this and from tAvo similar cases, communicated by Roth,3 it would seem to folloAv that not merely atrophy of the capillaries, but other mechanical obstructions in the renal circulation are capable of producing hypertrophy of the left ventricle. On the other hand, c, if this were true, the occurrence of hypertrophy of the left ventricle Avould be so frequent as to be nearly a constant con- dition, which we find from statistics is by no means the case. Accordingly it is most probable that we must seek for the true cause of hypertrophy of the heart in other conditions which are found at the same time, such as disease of the heart substance, an improper quality of the blood itself, and hence depraved nutrition, etc. 5. If I only now allude to sclerosis of great arterial tracts as a cause of hypertrophy of the left ventricle, it is because it has a double influence, and tAvo causes act in unison : a, The arteries, over a greater or lesser extent, are diminished in calibre, and hence the opposition to the Hoav of blood into a given region must increase ; and, b, by the diminution of elasticity in the arteries an important factor in the fonvard movement of the blood is lost, and accordingly must be replaced by increased activity in the heart,4 0. In the same way that contraction of the aorta and other arteries leads to an increased development of the left ventricle, so the same result may follow on dilatation of these vessels like- Avise from two causes: a, If the dilatation is considerable, the 1 Virchow's Archiv. Vol. LIII. * Beitrage zur. Exper. Pathol. Vol. IX. 1858. J AViirzburg med. Zeitschr. Vol. V. 1867. 4 Polotebnow (Berl. klin. Wochenschr. No. 35, 1867) relates four cases of hypertrophy of the left (and right) ventricle, which was accompanied by sclerosis in the aorta, in the a. tcries of the upper, and particularly of the lower extremities, etc. VOL. VI.—13 194 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. left ventricle must make a powerful exertion in order to force the current of blood through that which is retarded in the dilated portions. Krause ' describes a case where there was con- siderable diffuse dilatation of both carotids and of the abdom- inal aorta, with very noticeable hypertrophy of the left ven- tricle ; b, as such portions of the arterial system usually have lost their elasticity, there is the same failure alluded to above, in the force which drives the volume of blood forward. 7. Insufficiency of the aortic valve is doubtless the most fre- quent cause of hypertrophy of the left ventricle. If the valves do not close, then at each systole of the left ventricle it must expel not only the blood which has flowed into it from the left auricle during the diastole, but also, in addition, that Avhich has regurgitated from the aorta in the same time. In brief, it must with each systole send forward a larger quantity of blood than normal, and, in order to meet this demand, must suffer hyper- trophy. 8. Here we must consider what influence a general increase in the quantity of blood in the system must have on the left ven- tricle. Theoretically, an increase in the quantity of blood should increase the labor of the left ventricle ; but such a condition never lasts continuously for any great length of time, and fre- quent repetitions of it seem to be followed by no such conse- quences. As instances, I can only recall those people who are in the habit of drinking great quantities of water. As opposed to other nations, I consider the Germans great water-drinkers, but in Germany not only do we not find more hypertrophy than in other countries, but on the whole much less. In all these cases we are speaking of an excentric hyper- trophy, sometimes with a preponderance of dilatation of the cavities, and sometimes with preponderance of hypertrophy of the muscular tissue. 9. Pathological changes in the texture of the heart, such as myocarditis, endo- and pericarditis, and fatty degeneration must frequently be the cause of this disease of the left ventricle. In the last form doubtless the order of succession is the reverse, viz.: 1 Berl. klin. Wochenschrift. No. 11. 1873. HYPERTROPHY AND DILATATION. 195 the hypertrophied heart at last takes on fatty degeneration. In myocarditis the formation of indurated tissue especially leads to hypertrophy of the muscular tissue in its vicinity. If hypertro- phy of the left ventricle has followed upon adhesions of the heart and pericardium, it must have arisen, on the one hand, from an accompanying disease of the heart tissue, and, on the other, from an increased difficulty in movement caused by the adhe- sions, and the consequent increase in energy Avhich is thereby called forth. Hitherto we have only considered hypertrophy as a secondary disease. What can we say of idiopathic hypertrophy? With the great advances which have been made in pathological anat- omy, autopsies, where no cause can be found throughout the sys- tem for an hypertrophy of the heart, will become more and more rare, and only such observations as have been made in quite recent times Avill demand our consideration.1 We might term those cases idiopathic which arise from the use of certain poisons —as, for instance, from the excessive use of alcohol, coffee and tobacco, also those cases Avhich follow upon great mental excite- ment. Lancisi and Corvisart maintained this view with regard to the latter class of cases, and traced them back to palpitation occasioned by perturbation of mind; their vieAv is also generally accepted, and explained by the theory that there is increased irritation proceeding from the centres of innervation, and in this way there arises excessive action of the organ, with the usual results. Whether even in these cases there are not other dis- turbances, occasioned by the above-mentioned noxious influences which Avork with them, must remain undetermined. We cannot reckon amongst idiopathic hypertrophies those Avhich occur in pregnant Avomen (Larcher, Ducrest), or folloAving upon excessive bodily exertions, such as ascending mountains, or the fatigues of a campaign (Myers, Moinet, Thurn, Fraent- zel), or after repeated attacks of epilepsy, for in all these the 1 Bruzelius and Blix, Hygeia, 1870.—A young man of eighteen years had suffered since his ninth year from attacks of palpitation which came on suddenly, and lasted ten or twelve davs, and in one of these he died. On examination, no cause could be found for the hypertrophy of the heart. (It had not suffered fatty degeneration.) 196 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. ultimate cause of the hypertrophy must be sought in disturb- ances of the circulation. First, as regards the views of Larcher, who claimed that in the pregnant woman the arterial tract throughout the body had become elongated to supply the foetus, and accordingly increased power was required, these views received no support from his measurements, the results of which showed that they fell within the normal limit. The others may be explained on the supposi- tion, that in consequence of violent bodily exertions there arise frequent stases and congestions in the vessels, which are com- pressed by excessive contraction of the muscles ; and when the heart is able to meet the new demands, there follows hypertrophy; and where it fails, dilatation (of this latter, more hereafter). Now if we accept all the contributions on this subject as founded in truth, we shall yet be forced to the conclusion that there was a condition of the heart substance peculiar to the individual, which existed prior to the operation of the above causes, for, otherwise, how very frequent the observation of such disorders would be; and indeed some of the authors above men- tioned are astonished that such conditions have not been ob- served by them more frequently or in all campaigns. Although Traube has proved that in extensive muscular contraction there is increased pressure in the arterial system, yet in the periods of rest which intervene there must be an entire compensation, so that no evil results follow. No satisfactory explanation has yet been offered of the cause of hypertrophy in that complex set of symptoms which has been styled Basedow'1 s disease. Right Ventricle. — After the thorough consideration of this subject in connection with the left ventricle, we need now only to occupy ourselves particularly with an explanation of the causes of hypertrophy in the right ventricle. These are : 1. Stenosis at the origin of the pulmonary artery. 2. Narrowing of the calibre of the pulmonary artery by pres- sure from without, as by aneurisms of the aorta,1 tumors, etc. 1 I have before me a preparation which shows an excessively hypertrophied right ventricle taken from a patient fifty-six years of age, in whom I diagnosticated, during HYPERTROPHY AND DILATATION. 197 3. The cutting-off of capillary regions in the lung develops it in the most striking manner. Here not only does the hyper- trophy develop very gradual]}', but it reaches its highest develop- ment in these cases. In this class belong compression of the capillaries of the lung by pleuritic exudation (pneumo-thorax, as a rule, does not last long enough as such to cause it); tumors of any kind; curvatures of the spine ; rarefaction of the lung, and capillary compression in vesicular emphysema; obliteration of these capillaries by permanent infiltration, and by induration Avith or without bronchiectasis. 4. Clots in extensive portions of the pulmonary artery. 5. Over-distention of the system of the pulmonary artery, occasioned by incomplete evacuation of the pulmonary capil- laries into the pulmonary veins, ahvays leads to hypertrophy of the right ventricle, in consequence of the increased opposition to each neAv stream of blood thrown fonvard by that ventricle ; these over-distentions are most intense in those cases where there is disease at the left auriculo-ventricular opening. 6. The hypertrophy wiiich accompanies insufficiency of the semi-lunar valves of the pulmonary artery may be explained in the same manner as was the hypertrophy of the left ventricle, depending on a similar lesion in the aorta. 7. Atheromatous changes in the pulmonary artery will cause hypertrophy of the right ventricle, in the same two ways in which, as we explained above, it occasioned left hypertrophy where the same process Avas going on in the aorta (p. 193), and upon Avhich Klob1 has laid great stress. 8. As the same author has personally informed me, dilatation of the pulmonary arterial system, though it rarely occurs, will occasion hypertrophy of the right ventricle. Klob found, at an autopsy AA'hich he had recently made upon the body of a man forty years of age, a very considerable hypertrophy of this life, an insufficiency and stenosis of the pulmonary artery, and the autopsy showed the existence of these lesions, but depending upon a large aneurism of the ascending aorta (the size of the two fists) which crowded and thoroughly compressed the pulmonary artery. 1 Wochenblatt d. Ges. der Aerzte, 1865. 198 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. ventricle, occasioned by a notable dilatation, which was generally distributed through the system of the pulmonary artery. Hypertrophy of the auricles is much more rare than dila- tation of the same cavities, and is usually combined with the latter in such a manner that the dilatation is in excess, i. e., it is an excentric hypertrophy. This occurs in all those cases where the same pathological condition exists in an advanced stage in the ventricle of the same side, and it also occurs independently in stenosis of the right and left auriculo-ventricular openings respectively. Hypertrophy of the whole heart is found where there is a combination of several of the causes which served to develop hypertrophy in single portions of the organ. These are espe- cially : 1. Simultaneous disease at several of the openings. 2. Complications of valvular disease, with other disturbances in the circulation, such as aneurisms, or extensive sclerosis of the arteries, or with diseases of the lung, and the like. 3. Communication between the two ventricles. 4. General disease of the heart substance; e. g., following pericarditis or myocarditis and fatty degeneration ; in this class we may reckon chronic Bright's disease. Here we may best take up the question how it happens that, with an insufficiency of the mitral valves and subsequent hyper- trophy of the right heart, there occasionally folloAvs an hyper- trophy of the left heart as well, when this latter would seem to find no opposition to a complete emptying of its cavity by sys- tole, and accordingly would have no cause to become hypertro- phied. Friedreich explains it by saying that here, as in other important diseases, such as mitral stenosis, emphysema of the lungs, etc., there follow disturbances in the capillary circulation throughout the whole body, occasioned by dropsy, and these must be met by compensatory hypertrophy of the left ventricle. This explanation might hold when dropsy is present, but this is by no means always the case. The other mechanical theories are untenable, and especially that which claims that the current of blood must come with increased force from the auricle into the ventricle, which accordingly will dilate, and subsequently must, HYPERTROPHY AND DILATATION. 199 in compensation, become hypertrophied. There remains to us, then, only the following view, viz., that from the harmony of action in the two ventricles, and the unbroken continuity of the muscular fibres from one-half of the heart over on to the other, an affection of the muscular tissue of one side must have com- municated itself to the other. Hypertrophy of the heart is by no means a rare affection, for its presence at autopsies varies in frequency from 12 per cent., according to Willigk,1 to 18.4 per cent., according to van der Byl.* As regards the sex, the statistics are so variable that we cannot make any approximate ratio between the two. There seems, however, to be no special preponderance of either sex. This, of itself, is of importance in considering the etiology of the disease; for, if hypertrophy were so frequently occasioned by excessive physical exertions, then, without doubt, the prepon- derance would be immensely on the side of the male sex. In childhood the disease is very rare, and, when found, is usually congenital. It occurs especially in middle life and advanced age, and in the latter is without doubt a natural sequence of diseased arteries. Dilatation of the Heart. This is always a secondary disease, either occasioned : 1. By increased pressure within a cavity whose walls have not increased in thickness ; or by 2. Disease of the heart substance. At the close of this section we will speak of the possible occurrence of this disease idiopathically. We can best clear up the first point by citing two examples of the disease, after considering the special effects of the causes of excentric hypertrophy. In the left ventricle, dilatation is most beautifully developed in cases of insufficiency of the aortic valve. In consequence of the cavity being filled from two sides at once at each diastole (viz., by entrance of blood from the left auricle, plus that which regurgitates from the aorta), the walls of the 1 Prag. Vierteljahrschrift. Vol. XLIV. 2 Transactions of the Pathological Society of London, Vol. IX., 1861. 200 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. ventricle must submit to an increase in pressure for which they are not adapted and to Avhich they Avill gradually yield. Soon, however, by virtue of the compensatory power, innate in the heart, the condition changes into one of excentric hypertrophy, and now it generally depends on the nature and quality of the heart tissue which shall prevail, hypertrophy or dilatation. When the capillary circulation of the lung is over-distended, the right ventricle cannot discharge its contents Avith the usual facility into the pulmonary artery, and this stasis, together with the pressure of the blood which normally enters the cham- ber from the right auricle at the same time, will develop dilata- tion, and just so much sooner on this side than on the other as its muscular tissue is feebler and more ready to yield to in- creased pressure. Here, also, as we have described above, the condition soon changes into one of excentric hypertrophy. From what precedes, it is clear that the auricle on the same side as the ventricle affected, and which is subjected to the same influences, will undergo extreme dilatation. Enormous dilatations of the left auricle are found in cases where there is stenosis of the left auriculo-ventricular orifice. I have before me a similar dilatation of the right auricle, but even here asso- ciated with partial increase in its muscular substance, in a case of extreme stenosis at the orifice of the pulmonary artery with insufficiency of its valves. If the heart has lost its normal contractile power, through disease of its muscular tissue, then it will yield to the normal blood pressure, and the greater the advance the disease has made the greater will be the dilatation. First amongst the causes of this tissue change is myocarditis, whether idiopathic or following upon pericarditis ; second is fatty degeneration of the heart substance. After certain febrile affections, especially pyaemia, severe puerperal diseases, typhus, variola, scarlet fever, etc., the action of certain poisons, particularly of phos- phorus (Munck and Leyden),1 there ensues, on account of the breaking down of the muscular fibres of the heart into a molecu- lar detritus, and the subsequent relaxation of the muscular 1 Berl. klin. Wochenschrift, 1864, Nos. 49 and 50. HYPERTROPHY AND DILATATION. 201 tissue, an acute dilatation of the heart. Doubtless the changes Avhich occur in chlorosis may be explained in this manner. Of late years it has been held, and especially by Stark,1 that in severe cases of this disease we can make out an enlargement of the heart, which again gradually disappears with the return of health. Here also we must take up the question of an idio- pathic dilatation of the heart without any special disease of its muscular tissue. Various authors, Forget, Peacock, Maclean, Thurn, Thompson, Seitz, Black, Tread well, Fraenckel, have made the assertion that in the over-exertion incident to the fatigues of a campaign, and similar laborious occupations, the heart suffers and undergoes a dilatation of its cavities AAiiich may be followed by expansion of its orifices and subsequent in- sufficiency of the valves. The subject is most exhaustively treated in a very carefully-wrritten work by Seitz ; yet even this does not by any means convert me to a belief in idiopathic dila- tation. It Avould not be strange if it should sometimes happen that the heart Avas not in a condition to meet great additional demands upon its strength, and it should gradually succumb to the task, and suffer dilatation and all the subsequent ills ; but if this could take place without any disease of the heart sub- stance, Iioav frequent an occurrence it would be, for do not the mass of mankind live by severe physical exertion ? We can only believe, then, that certain hearts, /. e., abnormal ones, are not able to endure severe exertion. Wherein the disease lies, Avhether in some tissue change which we cannot recognize, or, what is quite probable, in disturbances in the innervation, Ave cannot at present determine. From the distinguished names cited as authorities by Seitz, we cannot doubt that the autopsies were conducted with the greatest care. But we must not forget that appearances quite similar to those quoted here are very frequently found in autopsies on drinkers. Now, porters and men of similar occupations, concerning AAiiom he treats, are very frequently hard drinkers. The same statement holds true for the view presented by Peacock, according to whom, the laborers in the Cornwall 1 Arch. f. Heilk Vol. I., 1860. 202 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. mines, from their constantly-repeated ascent of ladders, the disturbances thus occasioned in the circulation, and the demands for over - exertion of the heart, suffer from dilatation of its cavities, and even subsequent mitral insufficiency. But nature has so ordained, that when a healthy muscle is called on for extra exertion, it shall develop hypertrophy, and not atrophy, and, accordingly, a hollow muscle will not dilate. The hypertro- phy of the right ventricle shows in the most beautiful way how the heart is ready to meet an increased demand upon it. If the views of Seitz and Peacock were correct, how very frequently must dilatation of the right heart occur. Fraentzel confesses that his observations were made only in the campaign of 1870- 1871, and that he had made no similar ones in previous cam- paigns, and even here his entire number was only nineteen cases; finally, he allows that there must have been a certain deficiency in the resistance of the heart tissues to make the existence of dilatation with the hypertrophy possible. Pathology. Pathological Anatomy. It requires considerable skill and experience to recognize slight cases, either of hypertrophy or dilatation, and not to fall into the error, on the one hand, of mistaking a strongly-contracted] heart for one that is hypertrophied, or, on the other, a heart] relaxed and temporarily distended with blood for one which J dilated. It seems desirable to give the normal measuremen 1 and weight of the heart, in order to have a starting-point for til comparison of normal with diseased conditions of the org'J! According to Bizot, they are as follows : j' HALES. METRES. FEMALES. ■ Length of the heart..........................0.097 " 0.092 I Breadth " " ..........................0.107 " 0.099 1 Thickness" " ..........................0.038 " 0.031 V Length of the left ventricle....................0.066 " 0.072 jt Breadth " " " ....................0.119 " 0.104 1 Length of the right ventricle................. 0.084 " 0.075 1 Breadth " " " ..................0.188 " 0.172 HYPERTROPHY AND DILATATION. 203 Thickness of the Walla of the Left Ventricle— MALES. METRES. FEMALES. At the base..............................0.010 " 0.009 At the middle...............................0.011 " 0.010 Near the apex...............................0.008 " 0.007 Thickness of the Septum Ventriculorum— At the middle...............................0.011 " 0.009 Thickness of the Walls of the Right Ventricle— Base........................................0.004 " 0.003 At the middle ..............................0.003 " 0.002 Near the apex................................0.002 " 0.002 Breadth of the Auriculo- Ventricular Orifices— Left ventricle................................0.100 " 0 091 Right ventricle...............................0.122 " 0.106 Breadth of the Origin of the Aorta (above the valves).... 0 069 " 0.063 Breadth of the Origin of the Pulmonary Artery.........0.071 " 0.066 In children under eight years of age the left ventricle is relatively larger than in adult life (Gerhardt); this difference seems to depend upon a contraction of the aorta still remaining, which was originally formed at the point of emptying of the ductus Botalli. According to Bizot, the whole heart of children under eight years is relatively large. In new born children the walls of the right ventricle are as thick as those of the left; the true relation between the two is established later. Accord- ing to Bizot, all the dimensions of the heart increase up to the most advanced age, but most actively before the twenty-ninth year. The weight of the heart, according o Engel,1 for both ventricles without the auricles, is 220.6 grammes, according to Clendinning,2 for the whole heart, 300 gr. in males and 270 gr. in females. We have already said that the hypertrophy might affect the hole heart, or only one of its divisions, or even only an inte- al portion of that (e. g., only the papillary muscles, the conus teriosus, the septum, etc.). We also mentioned the classifi- •ion, both of hypertrophies and dilatations, and laid stress the statement that concentric hypertrophy was of rare urrence, simple hypertrophy not common, and the most fre- mt was the excentric form, sometimes in the ventricles and icles as well. When all portions of the heart are affected at same time, it often reaches an enormous size (cor taurinum). 1 Concerning some Pathologico-Anatomical Changes in the Heart. Wien. med. Wo- snschr. 1863-64. 2 Med. Chir. Transactions. II. Series HI. 1838. 204 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. The thickness of the Avail of the left ventricle may increase to 4 cm., that of the right to 2 cm., that of the left auricle to 0.7 cm., and that of the right to 0.5 cm. (Rokitansky). The greatest weight, according to Rokitansky, was 1120, and according to Hope 1250 grammes. When the left ventricle is hypertrophied, the shape of the heart is altered by its becoming elongated. If, at the same time, there is a dilatation of its cavity, then the sep- tum will be pushed over and will invade the right ventricular cavity. In hypertrophy of the right ventricle, the heart becomes broader and its apex is rounded off. This variation in the character of the change in shape, according as one or the other ventricle is affected, may be readily explained on the recoil- theory to which Scheiber * has already called attention. The en- larged heart is wont to assume a more horizontal position, and when the left hypertrophy preponderates, it extends tOAvards the left and downwards ; the diaphragm, upon which it rests to a greater extent than normal, may likewise be pressed doAvnwards. The texture of the organ is strikingly hard ; the tissue creaks and gapes open on section, and this is particularly striking in the right ventricle. The color in simple hypertrophy is dark red- dish-brown. Later on in the disease, when fatty degeneration has occurred in some portions, we find the heart substance sprinkled over with clearer, yellowish spots. Dilatation, with thinning of the walls, occurs most fre- quently in the auricles, when the distention, especially of the right, may be enormous, and terminates in complete disappear- ance of the muscular tissue, the endo- and pericardium coming into contact. If the borders of the orifices are not otherwise diseased, they are oftener enlarged at the same time, and the valves as well as the trabecule are thinned ; the tissue is pale, flabby, and easily torn, and on section the walls immediately collapse. The general view is, that the increase in mass of the muscular tissue is produced by an increased thickness of the primitive bundles, although it has not often been reduced to figures. Hepp,2 who puts the normal thickness of the primitive fibres at 1 Virchow's Archiv. Vol. XXIV. 2 Dissertation. Zurich, 1853. HYPERTROPHY AND DILATATION. 205 0.007 mm., found them to measure 0.03 mm. in an hypertrophied left ventricle. Friedreich found 0.025 mm. to be the mean of ten measure- ments of the hypertrophied left ventricle in a drinker. Accord- ing to Rindfleisch, the increase in volume takes place by splitting of the muscle cells. He formed his opinion on his finding some of these cells, containing, instead of one, two and even more nuclei, Avhich, according to Weissmann,1 indicates that splitting of the fibres in the long axis will follow. Zielonko,2 who carried out some studies concerning the nature of hypertrophy, found, in his experiments on frogs, on which he had partially ligated the aorta, causing a certain contraction of its calibre, that there followed an actual increase in mass of the muscles, which was not occasioned by enlargement of all the cells, but more particu- larly by increased growth and multiplication of free nuclei, wdiich might serve as material for new cell formation; this agrees Avith the statement of Zehetmayer on the same point, who found numerous cell nuclei. In hypertrophy of the heart in man, no true indication of it could be drawn from the size of the muscular cells (/. e., their dimensions bore no fixed relation to it), but, on the other hand, in atrophy of the heart the decrease in its volume was accompanied by a corresponding decrease in the diameter of the cells. It is an interesting fact, according to R. Lee,3 confirmed also by Cloetta,4 that in hyper- trophy of the heart there takes place also a thickening of the nerves; it is not certain, however, whether this arises from increase in their primitive fibres, or from a greater develop- ment of the connective tissue forming their sheath. Symptoms. Since hypertrophy and dilatation are usually secondary and not primary diseases, in the statement of symptoms, we must 1 Reichardt's Archiv. 1861. 2 Virchow's Arch. Vol. LXII. First Part. 1874. 3 Memoir on the Ganglia and Nerves of the Heart. London, 1851. 4 Virch. Archiv. Vol. V. 206 SCHROETTER.—DISEASES OF THE HEART SUBSTANCE. carefully distinguish between those which belong to the disease in question and those Avhich may be referred to the original disease. As regards inspection, we frequently find it stated (Gerhardt, Friedreich, Bamberger—Niemeyer and Dusch, par- ticularly in young subjects) that both general hypertrophy and that of the left ventricle cause an increased bulging over the heart, as if it were occasioned by the increased pulsation of the heart against the thoracic wall. I must decidedly object to this view ; I have seen no case of either of these diseases alone where such a bulging had ensued. As Skoda has already stated, this occurs only where these diseases are complicated with pericar- ditis, in A\Thich, as in pleuritis, there is a softened, spongy con- dition of the textures forming the chest-wall; and on this account, and particularly, also, from the increased traction of the inspiratory muscles, we have an abnormal bulging over the heart. The character of the impulse is one of the most striking symptoms of hypertrophy, especially in that of the whole heart and in that of the left ventricle. Very often we find it pushed downwards and further over to the left than normal, in the sixth, seventh, or even eighth intercostal space. Not unfrequently we may observe the whole change in position of the heart at each systole; while at the time of the greatest bulging we may observe retraction of the intercostal space lying over the apex of the heart, and also at the scrobiculum cordis. Displacement of the apex further to the left only indicates, as a rule, hypertrophy of the right ventricle, while dislocation to the left and down- wards at the same time indicates usually hypertrophy of the left ventricle. The character of the heart's impulse is very varied; the so-called heaving impulse is characteristic only of a left ven- tricular hypertrophy, in which very often, not only over the apex but also above it, the hand laid upon the chest will be raised with considerable force at each impulse. This phenomenon will be most distinctly observed by placing a stethoscope against the wall over the apex, and seeing how it will be thrown for- wards. Frequently the Avhole left side of the chest will be pushed over to the left with each systole, so that there ensues an actual heaving of the chest-Avail. In other cases the impulse is simply HYPERTROPHY AND DILATATION. 207 increased, and communicates a jarring blow to the head resting upon the chest-wall. Only in concentric hypertrophy, or at times of profound rest, or in diseases of the heart substance, does the impulse become weak. In hypertrophy of the right ventricle the jarring impulse is most evident between the apex and the lower portion of the sternum, and just here is strikingly distinct. This may be per- fectly well explained, as I have suggested above, on the recoil theory, for if the right ventricle has become hypertrophied, it is just here that the rebound must take place, while in hyper- trophy of the left ventricle the recoil from the aorta is directed toAvards the apex. In percussion of the heart, I hold firmly to the point, that we must ascertain accurately the place where the sound is abso- lutely dull, •/. 472 QUINCKE.—DISEASES OF THE ARTERIES. blood pressure above the contracted portion acts with greater force than usual upon the walls of the artery itself and on those of its branches, till both are so dilated that the outflow becomes as great as formerly, and so the uniformity of the blood pres- sure is restored. When the position of the contracted portion of the artery is withdrawn from observation, the abnormal col- lateral circulation may afford important diagnostic evidence. Small and perfectly unimportant arteries are found to possess a considerable diameter and to exhibit distinct pulsation ; they are often tortuous, and a purring thrill may be both heard and felt in them. Often they show signs of endarteritic disease, no doubt as the result of the abnormally high blood pressure exerted on their walls. At the contracted portion there is frequently audible a sys- tolic blowing murmur ; at other times this blowing murmur is continuous and only increased at each systole ; of course all this disappears upon the occurrence of complete obliteration. Beneath the contracted portion, the pulse is either not to be felt at all, or, at all events, it is much weaker than above it, because the equalization of the systolic increase of the blood pressure in the central artery only takes place gradually through the contracted portion and the collateral vessels ; hence the cir- culation in the peripheral parts, instead of consisting of a series of rhythmic waves, is more uniform in its character. Hence the characteristic form of the sphygmographic pulse curve is obliterated; the wave is lower, and both rises and falls gradually without any secondary elevations. It is recognized as more than usually delayed, partly because it is actually delayed by its collateral circuit, partly because the rounding of the summit of the pulse wave simulates the appearance of delay.1 There are but few arteries of a medium size (3-5 "mm. in diameter), the obliteration of which cannot be compensated by the development of a collateral circulation. The arteries of the spleen and of the kidneys are, however, exceptional in this respect; contraction of the splenic or of one of the renal arteries leads therefore to persistent anaemia and atrophy of the organ implicated, its tissue being gradually Vide Aneurism, p. 424. NARROWING OF THE AORTA. 473 changed into connective tissue. In other parts of the body, such as the extremities, contraction of the main artery may lead to anaemia, coldness, and atrophy, when the development of a collateral circulation is prevented by the diseased condition of the other arteries. CONTRACTION AND OBLITERATION OF THE AORTA AT THE JUNC- TION OF THE DUCTUS BOTALLI (DUCTUS ARTERIOSUS). This contraction is most usually observed just where the ductus arteriosus joins .the descending aorta, that is, a few cen- timetres below the origin of the left subclavian; more rarely it is met with a little above or below this point; this contraction may extend over a space of 0.5-1 ctm. in length, and may vary greatly in degree up to complete occlusion ; in the latter case the portion of the aorta lying above and that lying below are, at the part occluded, only connected by a mere cord of cicatricial tissue. The stricture is usually annular, as if formed by a du- plicature of the internal coats of the artery, over which the ex- ternal coat is continued; in other cases the vascular lumen is contracted on each side like a double cone towards the stricture. Apart from a dilatation of the aorta above the stricture, which is commonly found (being frequently associated with chronic in- flammation of the intima), other abnormalities (general contrac- tion, dilatation beneath the constriction) are but rarely seen;— the ductus arteriosus is usually closed. This condition has hitherto been observed in about sixty cases of all ages [up to ninety years. Craigie—Tr.], and more fre- quently among men than among women. In all probability it originates at a very early period of extra-uterine life in connec- tion with the shrivelling and obliteration of the ductus arteriosus. Under normal conditions, when the ductus arteriosus is closed, the blood supply of the lower half of the body, which has hitherto been conveyed by it to the descending aorta, must pass by the arch of the aorta, and consequently through the com- mencement of the descending aorta lying between the left sub- clavian and the ductus arteriosus, that is, through the connecting link between the fourth and fifth arteries of the primary vas- 474 QUINCKE.—DISEASES OF THE ARTERIES. cular arches (aorta and ductus arteriosus), and which, up till now, has been narrower than the rest of the aorta. Instead, however, of dilating to the calibre of the rest of the aorta, this so-called isthmus aortae sometimes remains contracted. By the shrivelling associated with the obliteration of the ductus arteriosus, an influence is exerted on the isthmus which results in its complete or incomplete occlu- sion (Rokitansky). It is true, indeed, that this explanation leaves the true cause of the phenomenon as incomprehensible as the physiological closure of the ductus arteriosus itself; and it is specially insufficient for the explanation of those cases in which the ductus arteriosus remains pervious. Still less satisfactory are the explanations of the stenosis by a thrombosis of the ductus arteriosus with extension into the aorta, or by compression of the ductus arteriosus by the left recurrent laryngeal nerve. According to Bochdalek, the obliteration of the artery is more probably brought about by proliferation of the fibre-cells of the media which gradually occlude its lumen. Possibly a local inflammation may have something to do with it; moreover, the stenosis is probably not always brought about in the same manner. [Whatever the cause of this obliteration, and it may vary, Rind- fieisch regards it as always occurring during uterine life while the heart is still single. For, as he says, " a contraction of the aorta in opposition to the high pressure of the blood would be contrary to all our experience of the mechanics of aneurism."—Path. Hist. Syd. Soc. ed. Vol. I. p. 297.— TV.] Along with this abnormality, other congenital malformations are not unfrequently found, such as supernumerary or incom- plete semi-lunar valves, deficiency of the cardiac septum, ste- nosis of the conus arteriosus from myocarditis, cleft palate, etc. Stenosis of the aorta leads, in the first place, to an increase of the amount and pressure of the blood in the arch of the aorta and its branches, which is usually neutralized by means of a collateral circulation leading to the lower half of the body. This occurs through the following channels : 1. Through the subclavian, internal mammary, superior and inferior epigastric arteries into the lumbar and femoral arteries. 2. By anastomoses between the first intercostal, the internal mammary, the dorsalis scapulae, the subscapularis, and the ex- ternal thoracic arteries, on the one hand, and the intercostal arteries, on the other. The arteries named are found to be correspondingly dilated and with thicker walls than usual. Should the collateral circulation be insufficient for the out- NARROWING OF THE AORTA. 47.5 flow of the blood, then the increased pressure produces dilata- tion of the arch of the aorta and its branches, and secondary dila- tation and compensating hypertrophy of the left ventricle. Symptoms. , Stenosis of the aorta in the region of the ductus arteriosus may run its course wholly without symptoms, and may be only accidentally discovered at the dissection of the body ; this hap- pens when it is moderate and its effects upon the circulation are compensated by the development of collateral routes and by cardiac hypertrophy. But even in such cases the diagnosis may be made by an objective examination, especially by the discovery of the dilatation of the above-named collateral arteries ; of these the dorsales scapulae, the epigastric and the mammary arteries may be both seen and felt as thick, often tortuous, pul- sating cords. A purring murmur often originates in these ves- sels, and may be both felt with the finger and heard on auscul- tation. Over the thorax this murmur is heard loudest over the intercostal arteries at the first and second dorsal vertebrae, also over the mammary arteries at the edges of the sternum, and it may be distinguished from a cardiac murmur by its postpone- ment relative to the cardiac impulse. In all the arteries coming off below the stenosis (provided they are not implicated in the collateral circulation), the pulse is feeble, slow, and delayed,1 or it may be entirely absent, since the pulse wave through the contracted portion is enfeebled and is propagated circuitously by collateral routes (by these alone when the occlusion is complete), and the blood stream is thus rendered more uniform (less pulsatory). This change of the pulse in regard to time and strength, which is specially remarkable in the femoral arteries, is decidedly the most important sign of this stenosis, since collateral dilata- tion in some cases cannot be discovered even when carefully sought for. Sometimes, at the back, over the site of the stenosis (the left 1 Vide Sclieele, Berl. klin. Wochenschr. 1870. 476 QUINCKE.—DISEASES OF THE ARTERIES. side of the fourth dorsal vertebra), and downwards from that point, a systolic murmur may be heard. The dilated arch of the aorta may often be felt in the tracheal fossa, and the existence of hypertrophy of the left ventricle, in the absence of other causes, must be regarded as of diagnostic importance. Should the stenosis be considerable, and the dilatation of the collateral arteries insufficient, or, should the hypertrophied heart be paralyzed, then the same symptoms occur as in chronic car- diac diseases : palpitation, dyspnoea, bronchial catarrh, dilatation of the right side of the heart, and all the phenomena of remora in the systemic veins. This disturbance of the compensation often depends upon the degeneration of the hypertrophied cardiac muscle ; at other times the aortic or mitral valves become dis- eased from the abnormally high pressure to which they are exposed. In a few cases, rupture of the aorta occurred, in others sud- den death from cardiac paralysis. Prognosis. Those affected with stenosis of the aorta may reach a very advanced age, and may die from some intercurrent disease. When, however, this condition has been recognized, when, there- fore, for the most part, the subjective signs of circulatory dis- turbance of any kind must have been present, the patients have generally died in a few months or years from dropsy, or sud- denly from rupture of the aorta, or paralysis of the heart. Treatment. When this condition has been early recognized, the cardiac complications which threaten life may be prevented or post- poned by leading a quiet life, free from violent exertion. In other respects the treatment must be similar to that for cardiac disease generally. NARROWING OF THE AORTA. 477 NARROWING OF THE AORTA, In its ascending portion from external pressure, is of rare occurrence, since tumors in the mediastinum, as well as aneurisms, are more apt to embrace the circumference of the vessel than to compress it. Narrowing of its calibre by an adherent thrombus is in this situation usually unimportant, and presents no other symptoms than those of endarteritis generally. Colin has observed sudden obstruction of the ascending aorta by a clot; in one case, perforation of a carcinoma cordis into the left ventricle; in another case, rupture of a myocarditic abscess gave rise to the formation of adherent thrombi, which, when suddenly broken off, obstructed the aorta ; the patients suddenly became pale, fell collapsed, and died instantaneously; the left heart was found to be greatly dilated. Narrowing of the descending aorta, both of its thoracic and its abdominal portions, is occasionally of congenital occurrence, and leads to precisely similar symptoms as those of contraction at the ductus Botalli; in forming the collateral circulation, all the intercostal arteries above the constriction convey the blood from the spinal column towards the mammary arteries ; all those beneath it transmit the blood in the contrary direction. The descending aorta is but rarely narrowed by any tumor, because of the amount of blood pressure present within it throughout its course. This narrowing may, however, be brought about by aneurism of the aorta itself, or by a carcinomatous mass (Velpeau). In one case related by Axenfeld1 the aorta of a kyphotic patient was narrowed by being bent. Obstruction by an embolus or autochthonous coagulum occa- sions a sudden or more gradual diminution of the amount of blood in the lower half of the body, and thus produces para- plegia or paresis, a feeling of numbness and pain, as well as an absence of the pulse and a lowering of the temperature in the same. 1 Bull, de la Soc. anatom. 1850. 478 QUINCKE.—DISEASES OF THE ARTERIES. Sometimes these phenomena are better marked in one ex- tremity than in the other, when the coagulum, situated at the place of bifurcation, obstructs the entrance of one iliac artery more than the other. When a collateral circulation is set up, all the phenomena of obstruction may gradually disappear ; at other times complete obstruction is followed by swelling, hemorrhage and gangrene in the lower half of the body. The phenomena attending the narrowing or obstruction of one common iliac are very similar to those just described, only of course limited to one side. When the collateral circulation is in such cases only imperfectly developed, we sometimes hive developed the peculiar phenomenon of intermittent lameness, as has been ob- served by Charcot (case of obliteration by aneurism) and Ollivier (case of oblitera- tion from an unknown cause, probably lues). In these patients there occurred occasionally, sometimes spontaneously, but always after long walking, a sensation of numbness and formication in the whole leg, also a cramped feeling of stiffness combined with weakness. The functions of the sensible and motor nerves seemed to suffer from the anaemia. One of the cases resulted in permanent paresis, the other in atrophy of the leg. Narrowing of the innominate, the subclavian, and carotid arteries at their origin, is by no means rare in arterio-sclerosis, and is manifested by smallness and delay or by failure of the pulse in the arm, or in the corresponding side of the head, more rarely by other functional disturbances, such as diminished temperature and slight numbness of the affected extremity, because even in the case of complete obstruction a collateral circulation is readily set up (by the vertebral, mammary, and inferior thyroid arteries). The subclavian arteries may also be narrowed or obstructed by a coagulum, an aneurism of the arch, or a tumor of the mediastinum or of the supra-clavicular lymphatic glands. Similar causes may produce narrowing or obstruction of the carotids, which in many cases causes no uneasiness whatever, but in others induces disturbance of the cerebral circulation, giddiness, convulsions, and paralysis. According to two cases observed by Kussmaul,1 this seems to depend upon defective development of the arterise communicantes of the circle of Willis. The author observed one case of obstruction of the left carotid with absence of pulsation from all its branches in a case of right hemiplegia, probably due to softening, but in it there was no post- mortem examination. In a case of obliteration, occurring at the origin of the superior mesenteric artery (in a man aged sixty), Tiedemann saw the collateral circulation carried out by the hepatic and the pancreatico-duodenal arteries. In a case related by Chiene2 of an aneurism of the abdominal aorta, the coeliac axis and both the mesenteric arteries 1 Deutsche Klinik. 1872. Nos. 50, 51. 3 Jour, of Anat. and Physiol. 1868. Nov. NARROWIXO OF THE PULMONARY ARTERY. 479 were obliterated; the collateral circulation was carried on by :—1. The phrenic and intercostal arteries on the left side. 2. The colic, renal, and supra-renal arteries on the left side. 3. The internal hemorrhoidal and the internal iliac arteries. NARROWING AND OCCLUSION OF THE PULMONARY ARTERY IN ITS TRUNK OR MAIN BRANCHES. (We here leave entirely unconsidered the very frequent, and often manifold, occlusion of the smaller branches of the pulmo- nary artery by thrombi.) Narrowing of the trunk or of one of the main branches of the pulmonary artery is of rare occurrence, as already narrated ; endarteritis is a very unfrequent event in the pulmonary artery ; narrowing of it, therefore, by an abnormal growth of the intima is quite exceptional. (Case of Tommasi: stenosis of the pulmonary artery at its bifurcation from cartilaginous thickening and calcification of the intima.) Aneurisms of the ascending aorta or of its arch, and also enlarged mediastinal or bronchial lymphatic glands may compress and narrow the pulmonary artery ; and this may also be brought about by cicatricial shrivelling of a patch of lung or of the bron- chial glands (Immermann). During life, narrowing of the trunk of the pulmonary artery gives rise to phenomena very similar to those produced by stenosis of its orifice in the region of the valves: to anaemia of the entire area of the pulmonary capillaries, and, as the result of that, to persistent dyspnoea with occasional exacerbations; to congestion, dilatation, and hypertrophy of the right heart, and as the consequence of this to cardiac palpitations and ultimately to general congestion of the systemic veins. The enlargement of the right heart is revealed by increased dulness and increased force of the cardiac impulse. The commencement of the pulmo- nary artery quite up to the beginning of the narrowed part may share in this dilatation the result of increased pressure (it may even as a consequence of this become secondarily affected with endarteritis); the second sound over the pulmonary artery is thus rendered abnormally loud and accentuated, while, when the 480 QUINCKE.—DISEASES OF THE ARTERIES. orifice itself is stenosed, the whole of the pulmonary artery is diminished in calibre, and the second sound is abnormally weak. In these, cases a systolic murmur produced by the stenosis is also audible, with its position of maximum intensity not therefore over the pulmonary valves, but above them (in Immermann's case, indeed, it was loudest in the second intercostal space on the right side); this may be propagated upwards to the neck, or it may be heard in the interscapular space close to the spinal column— when one of the main branches is more contracted than the other, it is probably most distinct on the side to which that is distributed. When the commencement of the pulmonary artery is dilated, its pulsation may sometimes be both seen and felt in the second intercostal space on the left side. It is important for the diagnosis to determine, besides the foregoing phenomena, the existence of glandular swellings, of an aneurism, or of pulmonary contraction (Immerman's case was one of stone-hewer's phthisis). The prognosis is unfavorable, and treatment of little use ; it must be similar to that of stenosis of the pulmonary orifice. Rupture and Perforation of the Arteries. Dissecting Aneurism. Rupture: Morgagni, Epist. LIII. 35 and 36.—H. Schnabel, Giinsb. Zeitschr. X. 1859. S. 421. Schmidt's Jahrb. 110. S. 243. Traumatic rupture of the healthy aorta.— Ollivier, Diet, en XXX. Vol. XXVI. 305. Rupture of the pul- monary artery.— Wallmann, Ueber Ruptur d. innern und mittlern Arterienhaut. Oesterreich. Zeitschr. fiir pract. Heilk. IV. 6, 7. 1858. Schmidt's Jahrb. 99. S. 230. Dissecting Aneurism : Laennec, Traite1 de 1'auscultation. 4. edit. 1837. in. p. 420. —Peacock, Edin. Med. and Surg. Jour. 1843, April and October. Edin. and London Monthly Jour. 1847, Nov. Experiments.—Peacock, Report on cases of dissecting aneurisms (eighty cases). Pathological Transactions. Vol. XIV. 1862- 63.—Peacock, Ibid. XVII. 1867. p. 50.— Rokitansky, Krankheiten d. Arterien. S. 41.—Do., Oesterreich. med. Jahrb. Bd. 16. 1837.—Do., Wochenblatt d. k. k. Ges. d. Aerzte zu Wien. 1866. No. 28.—Crisp, L. c. pp. 178 and 310.—Cases: 0. Barth, Arch. d. Heilk. XII. S. 253.1871.—Chauvel, Gaz. med. de Paris. 1866. No. 16.—67. Fischer, Diss. Wiirzburg. 1872 (two cases).—il Fagge, Med. Chir. Transact. Vol. 52. 1869.—F. E. Geissler, Ueber die als Aneurysma dissecans bekannte Ruptur der Aorta. Wiirzb. Inaugural. Diss. Bremen. 1862 (eighty- RUPTURE AND PERFORATION. 481 five cases).—Heschl, An. Diss, der Brust- und Bauchaorta mit Compression des Aortenlumens. Wien. med. Woch. No. 90. 1867.—Maudron, These de Paris. 1866.—0. Wyss, Arch, der Heilkunde. 1869. X. S. 490. Rupture of the arterial continuity may be occasioned by : 1. Wounds. In peripheral arteries these are most frequently caused by stabbing or cutting instruments ; but in the aorta this is of rarer occurrence. A preparation in the pathologico-anatomical collection at Berne exhibits a wound of the abdominal aorta by a dagger-knife, which had gone through one of the vertebrae. Injuries to the arch and to the aorta descendens by a set of artificial incisors and hy a piece of wood, which had stuck in the oesophagus, have been recorded by James Duncan and Kreyser.1 Wounds of the intima of the smaller arteries (at the base of the brain and in the mesentery), seem to be occasionally pro- duced by embolic calcareous plates coming from the cardiac valves or the intima of the aorta, and lead to the formation of aneurisms (Ponfick). The coats of the arteries are capable of being ruptured by direct violence (contusion or laceration), just as they also are by violent concussion of the whole body, by a fall from a great height, etc. The intima seems to be thus singularly easily rup- tured, as we are taught by the results of ligature of the arteries. The experience of Wallmann has proved that a violent blow from a blunt weapon ruptures during life as well as after death, when the arteries are tense and full—first of all the intima, next the media, and with greatest difficulty the ad- ventitia. In this way the great arteries of the extremities and even the aorta itself may be ruptured. Thus Morgagni saw the aorta descendens torn across by a blow from a stick on the back. 2. Rupture is favored by a certain degree of tension of the arterial coats ; therefore the filled arteries of the living body are more readily torn than the empty ones of the cadaver. Tension of the arterial coats from the blood-pressure alone may lead to rupture, especially where these coats are degener- 1 Vide Ungues, Lyon medical. 1870. No. 17. Vide also Northern Jour, of MoJ. 1S44. p. 15. VOL. VI__31 4S2 QUINCKE.—DISEASES OF THE ARTERIES. ated in any way, and the blood-pressure is increased by hyper- trophy of the left ventricle and by increased force of the cardiac action. 3. Disease of the arterial coats is of the greatest importance in regard to the production of rupture. Suppuration or carci- noma only rarely implicates an artery ab externo. Ogle saw ulceration of the abdominal aorta as the result of caries of two lumbar vertebra?.1 Bucquoy and Lancereaux'2 observed perforation of the aorta descendens produced by epithelial carcinoma of the oesophagus. The aorta was ulcerated, but not carcinomatous; vomiting of blood occurred. Rokitansky and others have seen ulceration of the femoral artery the result of the suppuration of a bubo; Crowfoot, ulceration of the pulmonary artery from an abscess of the lung.3 On the other hand, the arterial coats are not unfrequently destroyed by the action of the gastric juice; this happens most frequently to the gastric artery itself, but the splenic artery and others may be opened into by a gastric ulcer. Stich 4 has recorded the opening of the (atheromatous) abdominal aorta by an ulcer in the lower transverse portion of the duodenum. The old woman died eighteen days after the commencement of the haematemesis. Abnormal thinness of the walls, either congenital or the gradual result of dilatation above a contracted part (as, for instance, at the isthmus aortae), predisposes to rupture, whether that be finally produced by violence or occur "spontaneously'' from the blood pressure. Fatty degeneration of both the internal coats frequently, but chronic endarteritis more frequently still, gives occasion to rupture of the arteries, insomuch as they lead to ulceration of the intima, to brittleness of the intima and media, as well as to thinning of the arterial coats by atrophy and dilatation. With arteries so predisposed, violence or increase of the blood pressure very readily produces rupture. 1 St. George's Hosp. Rep. 1867. II. p. 375. 5 Bull, de la Soc. anatomique. 1855 and 1861. 8 Medico-chir. Transactions. XXVI. p. 154. * D. Arch. f. klin. Med. 1874. XIII. S. 191. RUPTURE AND PERFORATION. 483 Should the rupture be complete and embrace all the three coats, then the blood escapes either into an adjoining cavity, the pericardium, pleura, etc., or into the surrounding cellular tissue, within which it both forms and fills a hollow, larger or smaller, according to the amount of resistance present. In many cases the rupture at first is only incomplete, gener- ally only implicating the intima ; by and by, under the influ- ence of the blood pressure, the external coats stretch and at last give way ; should this occur very gradually, then an aneurismal sac is formed by condensation of the surrounding connective tissue; should it happen after hours only or days, then the re- sults are the same as in simple rupture. Sometimes the blood forces its way through the rupture not only outwards, but also between the arterial coats, so that the adventitia is separated from the media by a blood sac, forming a dissecting aneurism. At other times the blood forces its way between the layers of the media, so that the external wall of the sac is formed by the adventitia plus one of the layers of the media. According to Peacock, the latter is the rule, since he could only produce dissect- ing aneurisms artificially in the dead body by injecting water, when the media had been imperfectly cut through ; when it had been completely divided, the only result was diffuse infiltration of the neighboring tissue; a true sac is, however, always produced when, as so often happens in arterio-sclerosis, the adventitia is condensed. Vide supra, the experiments on animals in regard to the artificial production of aneurism, p. 410. The blood sac lying between the arterial coats is often of con- siderable size, embraces a large part of the arterial circumference, and extends for some distance along it, as far, for instance, in the aorta as to its bifurcation. Finally, the rupture may become complete by the giving way of the adventitia, or a second com- munication with the arterial lumen may be formed by the rupture of the inner layer of the sac. In certain rare but well established cases a cure has resulted by the formation of coagula on the inner surface of the adventitia, and the thickening of the latter coat. In one case of dissecting aneurism of the aorta, described by 484 QUINCKE.—DISEASES OF THE ARTERIES. Helmstedter,1 in which the media was for a considerable extent divided into two layers, the inner surface of the sac, both on its central and peripheral sides, was covered by a layer of connec- tive tissue of recent formation, by which the origins of the inter- costal arteries were partly narrowed, and partly occluded. The rupture is usually transverse (especially in the ascending aorta), sometimes oblique or parallel with the axis of the vessel. Its length at the most is two-thirds of the arterial circumference; usually it is less (Peacock). Spontaneous rupture of the arteries (inclusive of dissecting aneurisms), like chronic endarteritis, occurs most commonly in advanced life, and most frequently in the aorta, particularly in its ascending portion ; rupture takes place most frequently into the pericardium. Rupture of the pulmonary artery has been occasionally seen, but dissecting aneurism never. Symptoms. In rupture of the aorta, as in rupture of the heart, death is preceded by a feeling of anxiety, pallor, and loss of conscious- ness, when the rupture is large and the blood escapes freely into any cavity (pericardium, pleura, or peritoneum); when the open- ing is small and the bleeding takes place into the mediastinal or retro-peritoneal connective tissue, the phenomena of internal hemorrhage do not occur with such lightning-like rapidity ; the effused blood may be recognized by percussion, and by its pressure may injuriously affect the cardiac force and the respira- tion ; may occasion violent pain, and by compression of arteries or nerves may give rise to local disturbances of the circulation, motility, or sensibility in one of the extremities. Disturbance of the cerebral and renal functions has also been observed as the result of obstruction to the blood-flow thus produced (Peacock). The patients have themselves sometimes had a sensation as of something giving way internally. Such a slow progress is most apt to be observed in cases of dissecting aneurism, and in them death may follow in a few days, 1 Diss. Strassburg. 1873. RUPTURE AND PERFORATION. 485 complete rupture, or, in spite of the threatening symptoms, a cure may occur in certain rare cases, or finally the symp- toms may ultimately come to resemble those of a simple aneu- rism. A dissecting aneurism of one of the main branches of the aorta may be sometimes recognized by palpation, from the con- sequent change in the form of the artery. The treatment is the same as that of rupture of an aneurism. A case narrated by Verneuil is very remarkable,1 in which, after being run over by a railway wagon, the patient had both the internal coats of the left internal carotid torn across (apparently by violent twisting of the head). Thrombosis of the carotid as far as the middle cerebral artery, softening of the temporal lobe, and paralysis of the right side resulted; death occurred in five days. 1 Bull, de l'Acad. de Med. 1872. No. 2, p. 46. DISEASES OF THE VEINS. Literature of the subject generally and literature of phlebitis. Vide the handbooks of pathological anatomy by Cruveilhier, Forster, Rokitansky, antl others; and the handbooks of special pathology and of diseases of the heart, by Bamberger, Bouillaud, Corvisart, Duchek, Friedreich, Hope, Jaccoud. Bollinger, Eudophlebitis verrucosa of the portal vein of the horse. Virch. Arch. Bd. 55. S. 279. 1872.—Bouillaud, Arch. gen. 1824. Dec. 1833. June.— Crisp, Treatise on diseases of the bloodvessels. 1847.—Duchek, Krankheiten der Venen. Wiener. Allg. med. Zeitg. 1863.—-Do., Prager Vierteljahrschrift. Bd. 41. S. 109. —John Hunter, Transact, of the Soc. for the Improvement of Med. and Chir. Knowledge. 1793. Vol. I. p. 18.—Lee, Inflammation of the pulmonary veins. Med. Chir. Transact. XIX. 44.—Meinel, Archiv f. physiol. Heilkunde. 1848.— Paget, On gouty and some other forms of phlebitis. Bartholomew's Hosp. Rep. 1866. II. p. 82.—Do., Clinical lectures and essays. 1875. p. 292.—Tuckwell, Bartholomew's Hosp. Rep. 1874. Vol. X. On clotting of blood in gout and chlorosis.— Pelvet, Phlebite rhumatismale. Gaz. des Hop. 1866. No. 28.— Puchelt, Das Venensystem. II. Aufl. Heidelberg. 1843. Stannius. Ueber Ver- schliessung grosser Venenstamme. Berlin. 1839.— Velpeau, De la phh?bite. Paris. 1829.— Virchow, Arch. Bd. I. Spec. Pathol. Bd. l.—C. 0. Weber, Billroth, Pitha's. Handb. d. Chir. II. 2. p. 97.— Zahn, Ueber Thrombose. Virch, Arch. 1875. Phlebitis. 1. Acute Phlebitis. Acute phlebitis generally begins in the adventitia with red- ness and swelling of it, as well as of the surrounding connective tissue; sometimes there is only serous infiltration, at others a denser swelling with cell proliferation. The media and intima may also be implicated in these changes, and may become cloudy and thickened. By and by there occurs either complete absorp- tion of the exudation, or it may become organized with a new growth of connective tissue in the external coats and the adjacent ACUTE PHLEBITIS. 487 tissue (chronic, sclerosing phlebitis), or the exudation may soften with a more or less copious formation of pus, the normal ele- ments of the venous coats becoming granular and breaking up into a fatty detritus. In the former case the iutima is more rarely, in the latter more frequently, altered, either thickened and plicated, or projected like a pustule by the solid or fluid exudation in the media ; or it may partly fall into molecular detritus, and partly disappear by ulcerative absorption due to the pressure of accumulated pus. Xery early in the disease a blood coagulum may form on the diseased part of the venous wall—so soon, namely, as the endo- thelium of the intima has become altered in the slightest degree from its normal (Zahn); coagulation occurs therefore more read- ily in the destructive than in the sclerosing form of inflammation. According to the nature and intensity of this inflammation, according to the size of the vein affected and the force of its blood current, this coagulum either remains adherent to the wall or obliterates the lumen of the vessel and undergoes further changes, which lead either to its organization or to softening, and which vary in character with the nature of the phlebitis. When the intima is destroyed, it depends upon the extent and firmness of the coagulum whether the contents of the inflamed part are at once let loose, or whether they are gradually mingled with the blood current and are swept away by it. Though the phlebitis just described is primary in its occur- rence, and the thrombosis a secondary and by no means necessary result, yet, on the other hand, we frequently meet with precisely a reversed condition : a primary thrombosis and a secondary phlebitis, which is then primarily associated with important changes of the intima, and will be particularly described under the heading of "Thrombosis." From the thinness of the venous coats, we cannot readily subdivide phlebitis, as we do arteritis, into inflammation of the external, middle, or internal coats. The predominant importance of the individual coats in the various forms of venous in- flammation may be gathered from what has been already said. The most common cause of phlebitis is inflammation in the neighborhood of the veins : suppuration of the cellular tissue (as 4S8 QUINCKE.—DISEASES OF THE VEINS. the result of pelvic, intermuscular, or subcutaneous cellulitis) following bruises, fractures of the bones, or operations; or direct injury to the coats of the veins by bruises, lacerations, ligature, or wounds from cutting-instruments, as in venesection. Further, primary thrombosis of a vein, as already said, fre- quently leads to inflammation of its coats. Previous dilatation, varicosities, or chronic inflammation of the coats of a vein dis- pose to acute phlebitis. (Primary) phlebitis frequently occurs without any apparent local cause ; e.g., in pysemia, or in gout. In such cases it is frequently associated with other gouty inflammations, especially in the lower extremities, according to Paget. The same author further describes cases of widely diffused phlebitis, which he regards as having been produced by putrid infection from sewer gases. Pelvet has an idea that there is an acute specific rheumatic phlebitis, anal- ogous to the endocarditis which accompanies acute rheumatic affections of the joints. The symptoms of acute phlebitis are in themselves of a very indefinite character; they resemble on the one hand the symp- toms of inflammation of the parts in the neighborhood of the vein, and on the other those of thrombosis, presently to be referred to. According to the extent of the inflammation of the surround- ing connective tissue, there is either only a uniform diffuse infiltration to be felt, or the periphlebitic thickening of the tissues runs along the inflamed vein, and is felt like a cord, pro- vided the vein is superficial; at the same time the vein is painful on pressure or movement. Thrombosis of a vein can only be recognized by palpation in trifling degrees of inflammation of its coats, at other times it is revealed by consecutive disturbances of the circulation (venous congestion, oedema, lowering of the temperature). Fever may be present or not. The former is the case when the inflammation of the surrounding tissues is somewhat exten- sive, or when the inflammation has led to destruction of the coats of the vein and to the entrance of the resulting detritus into the circulation ; while, on the other hand, a limited phle- bitis, or one tending to organization, whether the accompanying CHRONIC PHLEBITIS. 4S9 thrombosis has been primary or secondary, runs its course with- out any or with but little fever. The entrance of pus or of the detritus arising from tissue destruction into the circulation is usually followed by metastatic inflammations, particularly in the lungs. Treatment.—In every case in which suppuration occurs in the neighborhood of a vein, the prevention of phlebitis is a primary and most important object, and this necessitates the most careful and painstaking treatment of the parts primarily diseased, the opportune opening of abscesses, removal of foreign bodies, etc. Should the inflammation approximate a vein, or should it be necessary to wound a vein in any operation (even only in venesection), then we must still more carefully en- deavor to prevent the entrance from without of any infective material, because the entrance of such into a vein directly, or by means of the breaking down of a thrombus, leads to the danger of general infection. On the other hand, a benign phlebitis, which leads to thickening of the coats and the formation of an organizable thrombus, is a process often necessary for the heal- ing of a wound, and has a tendency to prevent the occurrence of infection. The detraction of blood by leeches applied along the course of the inflamed vein, as well as the application of cold, are in most cases unnecessary, and are only indicated by the occur- rence of a considerable amount of pain and swelling. On the other hand, poultices tend to relieve both pain and tension and to favor absorption. The envelopment of the part affected in cotton wool, with or without repeated frictions with mercurial ointment, is recommended by some. Under all circumstances, the part affected must be so placed as to secure the fullest possible rest, to prevent tension or pressure on the inflamed vein, and to promote the return of the blood from the peripheral parts by means of the collateral circulation and the influence of gravity. 2. Chronic Phlebitis. Chronic phlebitis occurs either as the result of an acute in- 490 QUINCKE.—DISEASES OF THE VEINS. flammation, or in cases of permanent dilatation (from congestion, the influence of collateral flow, varicosity, etc.), or in cases of primary thrombosis. It leads to thickening of the coats, espe- cially of the external layers, whilst the intima remains intact. In the parts affected there is proliferation of the nuclei and hyperplasia of the connective tissue ; in the media there is also hypertrophy of the muscular coat ; the vasa vasorum are also strongly developed as far as the media, and often so dilated that in the coats of the vein there are venous sinuses of the dimen- sions of cuticular veins. The intima is, however, unaltered, and its epithelium uninjured. In opposition to this description of varicose veins (from the investigations of Soboroff and others), Cornil states, as the result of his own independent examina- tion of varicose veins, that the new formation of the connective tissue chiefly takes place between the media and intima; in other respects his observations agree with those just stated. Secondly, we may have a chronic endophlebitis, analogous to endarteritis, in those veins which have been exposed to great pressure, as in the pulmonary veins in disease of the mitral valves, in the large systemic venous trunks in cases of obstruc- tion to the emptying of the right ventricle, or in peripheral veins in aneurism by anastomosis. The anatomical alterations in endophlebitis are analogous to those of endarteritis, and like these result in thickening, calci- fication, rarely in fatty degeneration and atheromatous destruc- tion of the intima, and are secondarily accompanied by chronic inflammation of the external coats, or by calcification of these. In it the intima is beset at times with isolated plates, and at others it presents an extensive diffuse thickening, so that the inner coat of the vein presents an appearance like that of an artery. Clinical symptoms are absent in most cases of chronic phle- bitis. After a preceding attack of acute phlebitis, the persist- ence of the disease in a chronic form may be suspected, from the continuance of congestion and dilatation ; but we can only ascertain this certainly in superficial veins, in which, besides a HYPERTROPHY, ATROPHY, ETC. 491 uniform or varicose dilatation, we can very often feel a thicken- ing or calcification of the walls. Most commonly attention is first directed to the existence of this affection, by the fact that chronically inflamed veins are specially predisposed to thrombosis and to acute phlebitis. The treatment must be directed to the prevention of such complications, as well as of the further progress of the chronic inflammation, by warding off every source of injury or of ex- ternal irritation. The cause of the venous congestion must therefore, as much as possible, be removed, and the part affected must be so placed as to favor the return of the venous blood by means of gravity. The endophlebitis verrucosa, observed by Bollinger in the portal vein of horses, possesses an anatomical interest. In these cases, the internal surface of the portal system (apparently as the result of sclerosis of the perivascular connective tissue) exhibits, over several square centimetres, a velvety appearance produced by minute warty elevations of the intima, which contain, besides almost homogeneous con- nective tissue, connective-tissue cells, and round cells, but no vessels. Hypertrophy, Atrophy, Degeneration, Neoplasms of the Venous Coats. Pure hypertrophy, with a uniform thickening of the coats, with dilatation, elongation, and tortuosity of the venous tube, occurs in veins which have been long engaged in carrying on a collateral circulation. Further, hypertrophy of the venous coats, as just described, occurs in connection with chronic inflammation, and as one of its results, especially when accompanied by persist- ent increase of the pressure of the venous blood. Similar conditions may lead to atrophy of the walls, when combined with considerable stretching and dilatation of the venous tube. Persistent external pressure, persistent diminution or cutting off of the blood stream from a vein (as, for example, in atrophying organs), leads also to atrophy of its walls. The venous coats are less subject to degeneration in general than the 492 QUINCKE.—DISEASES OF THE VEINS. arterial coats; thus fatty degeneration is somewhat rare, but calcification is more common. By it, plates or rings are formed, which are commonly imbedded in considerable numbers in the venous walls, especially in dilated veins, in the inferior extrenr- ties. Calcification of blood clots (phleboliths) also frequently occurs in these situations. In extensive amyloid degeneration the large systemic venous trunks, and also the portal vein, are often affected, sometimes throughout the entire thickness of their coats, at others only the media or the vasa nutrientia. Of these degenerations we can only recognize—and only in the superficial veins—hypertrophy, atrophy, and calcification, which alter the resistance of the venous tube, in relation to the finger palpating it, as well as its extensibility in regard to cen- tral compression. Atrophy favors rupture from violence or sudden increase of the blood pressure. Carcinoma affects the veins almost always only secondarily, spreading from the neighborhood, but attacking them more fre- quently than the arteries, on account of the thinness of their walls. Sometimes the carcinoma breaks through into the lumen of the vein, and grows there, producing thrombosis ; sometimes coagulation of the blood occurs previous to the breaking in of the carcinomatous growth. In this way both large and small venous trunks may be affected by carcinoma. Sometimes the carcinoma grows forwards cylindrically within the venous lumen, as in the portal vein. Should particles of the cancerous mass be swept away by the blood stream, they may, as emboli, give rise to secondary cancers (in the lungs or liver). The results and symptoms during life are the same as those in simple thrombosis of the veins. Perl and Virchow1 have described a primary sarcoma of the vena cava inferior in a woman aged thirty-four. It was a myosarcoma with giant cells, and formed several tumors, the size of the fist, in the space between the kidneys and the lower edge of the liver. The vena cava was surrounded by the growth, and, as well as the renal veins, was almost completely filled by it; the aorta was compressed. 1 Virch. Arch. Bd. 52. 1871. SYPHILITIC DISEASE. 493 Syphilitic Disease of the Veins. Oedmansson, Cases of syphilitic disease. Nord. med. Ark. I. 4. (Virch. Jahresber. 1869. II. S. 561.)—Schiippcl, Ueber Periphlebitis syphil. bei Neugebornen. Arch. d. Heilk. XL S. 74. 1870.—Heubner, S. 169.—Birch-Hirschfeld, Beitr. z. pathol. Anat. d. hereditaren Syphilis Neugeborner. Arch. d. Heilk. 1875. XVI. S. 166. — Winckel, Ber. u. Studien aus deni kgl. sacks. Entbindungsinstitut. 1875. S. 307. A circumscribed disease of the intima, similar to that described by Heubner in the arteries, especially those of the brain {vide supra), has been observed by Anderson and Birch- Hirschfeld in the umbilical vein within the cord, and has been by them connected with congenital syphilis. But, indeed, in some of these cases no other more certain proof of the existence of syphilis could be ascertained. Oedmansson regards this affection of the intima of the umbilical vein, even in actual syphilitics, as still belonging to atherosis. This disease is in so far of considerable importance that the stenosis of the umbilical vein, thus produced, is, according to Oedmansson and Winckel, a frequent cause of the intra-uterine death of the foetus in syphi- litic women. In new-born children, Schiippel has also observed a peculiar alteration of the portal vein at its entrance into the liver, pro- duced by syphilis. In these cases the vein was changed into a thick dense cord with a much con- tracted lumen; its coats consisted of a central grayish yellow opaque zone, and a peripheral one, gray and more transparent, which gradually passed without any definite boundary into the surrounding tissue; a microscopic examination exhibited a fibrous tissue, finely granular masses, and many partially atrophied lymphoid cells. This gummy peripylephlebitis affected either the tiunk of the portal vein or one of its main branches, and extended along the capsule of Glisson into the liver, so that this organ appeared to be permeated in every direction by firm, fibrous, and, for the most part, perfectly solid cords. In the three cases observed, the umbilical vein was unaffected; in one, the ductus venosus Arantii was also diseased. In this solitary case the ductus hepaticus was also compressed by the gummy inflammation, so that (five days after the birth, and three days and a half before death) jaundice from1 obstruction was produced. In the second case, icterus was also present from three to five days before death; the third child only lived eight hours. The spleen in 494 QUINCKE.—DISEASES OF THE VEINS. all the three cases was considerably enlarged. In one case there was intestinal hem- orrhage, in the other peritoneal effusion. Dilatation of the Veins. Briquet, Arch. gen. VTI. pp. 200 and 396. — V. Cornil, Sur 1'anatomie pathol. des veines variqucuses. Arch, de physiol. 1872. p. 602.—John Marshall, On the extirpation of varicose veins. Lancet. IV. 1875.—Ravoth, Ueber Druckbehand- lung d. Varicocele und d. Phlebectasie. Berl. klin. Wochenschr. 1874. S. 222. 1875. S. 317.—Soboroff, Ueber den Bau normaler und ektatischer Venen. Virch. Arch. Bd. 54. H. 3. 1872.—P. Vogt, Beh. d. Varicen mit Ergotininjectionen. Berl. klin. Wochenschr. 1872. No. 10. We have much less accurate information as to the normal diameter of the veins than as to that of the arteries, because in them the physiological distention is subject to much greater variation, while the tension of the contents has a much greater influence. Indeed, it seems as if the great venous trunks, from their distensibility, were intended to serve as reservoirs for the blood under certain physiological conditions, such as limitation of the peripheral circulation (by cold, etc.). The diameter of the veins, therefore, varies very considerably within physiological limits, according to the amount of blood present in the individual. The dilatation is either uniformly cylindrical (with or with- out coexisting elongation, and hence tortuosity), or it is circum- scribed and saccular (varix, corresponding to the usual forms of aneurism in an artery), which like an aneurism may either affect the whole of the circumference of the vein, or only a part of it, and at one time is attached to the vein by a narrow neck, at another by a wider one ; it may develop secondary bulgings, and may vary in size from a pin's head to a walnut. These varices are most frequently found on the central side of the venous valves ; when venous congestion sets in, the venous tube is by means of the valve temporarily changed to a cul-de-sac. Varices much more commonly than aneurisms occur together in considerable numbers. This latter form of dilatation is not commonly found alone, but associated with the cylindrical. The coats of the dilated veins are sometimes normal, more frequently thinned, or thickened by chronic inflammation {vide DILATATION.—ETIOLOGY. 495 svprd). Very often both thinning and thickening are simultane- ously present in different parts of the vessel. The surrounding connective tissue is not unfrequently in a state of chronic inflam- mation, sclerosed, and the vessel thus adherent to surrounding tissue is less mobile than usual, or, if it be considerably dilated, the pressure of the neighboring tissues, such as the skin, or the subcutaneous cellular tissue, may cause it to atrophy in circum- scribed patches. The vein is often simultaneously elongated, and therefore tortuous. From these tortuosities, as well as from the projecting varices, the vein assumes a necklace- (rosary-) like appearance ; when the individual projections come in contact with one another, or with those of a neighboring vein, their coats may atrophy at limited portions, and so give rise to abnormal communications. The valves in the dilated veins are also distended and subsequently very often insufficient, atrophic, or fenestrated. Blood coagula, which more or less complete^ occlude the lumen of the vessel, are of frequent occurrence in dilated veins, especially in the varices and in the peripheral trunks. Etiology. "Dilatation of the veins is chiefly brought about by the per- sistent accumulation of blood in the veins, whether this is caused by obstruction to the onward flow (congestion), or whether it happens, because by the occlusion of certain veins a larger quantity of blood than usual is forced to pass through other collateral vessels. Dilatation of the veins is consequently present in all cases of disease of the heart or lungs, accompanied by con- gestion of the right side of the heart, or by diminished aspiration of the venous blood towards the thorax. In such circumstances those veins are chiefly dilated which pass their blood onwards in direct opposition to the force of gravity, such as the veins of the lower half of the body. Long-continued retention of the body in one uniform position may also produce dilatation of the veins of certain parts; con- tinuous standing, for instance, occasions dilatation of the veins of 496 QUINCKE.—DISEASES OF THE VEINS. the lower extremities, especially of the legs. Obstruction to the outflow from certain venous trunks (by the pressure of a tumor, or of a contracted muscle) causes dilatation of their radicles ; thus we have dilatation of the hemorrhoidal veins as the result of pressure on the portal vein. Further, the veins are dilated when flushed with arterial blood, as in arterio-venous aneurism. A relaxed and atonic condition of the surrounding tissues, which gives the venous coats but little support, favors the oc- currence of every form of dilatation. It is for this reason partly, and partly simply because of the increased flux of blood through the part, that we so often find venous dilatation in connection with repeated local hypersemiae, as well as in the neighborhood of new formations. It has been also generally supposed that a diminution of the tone of the venous coats themselves, a paretic condition of the muscular coat of the veins may assist in producing dilatation ; but though this is both possible and probable, it has not yet been certainly proved. A hereditary disposition to venous dilatation, especially in cer- tain areas, must be regarded as certain. Sometimes venous dilatations—congenital or acquired—are found without evident cause to account for them. Venous dilatations are of very common occurrence in middle life, both in men and in women ; in children and old people they are not so frequent. Symptoms. Dilatation of the veins is generally slowly developed, so that the vessels, as we can readily see in the cuticular veins of the lower extremities, only gradually, by long continuance of the standing posture, attain an abnormally great diameter. They then appear as more or less tortuous, knotted cords, which dis- appear on pressure or in certain positions of the body, but which reappear or are more largely developed when the onward now> of the venous blood is obstructed. These vessels appear of a DILATATION.—SYMPTOMS. 497 normal or bluish color, according to the thickness of their coats and of the overlying skin. In the part of the body affected (the lower extremities, the testicles, etc.), the patients have a sensation of weight and ful- ness, and it may be swollen or even cyanotic when the smaller veins are turgid, but always cool. The neighboring organs, such as the testicles, may be atrophied by the venous pressure. Even the venous coats themselves may yield to the continuous disten- tion, and at last give way on some trifling occasion, thus giving rise to hemorrhage, either externally or into the connective tissue. Finally, thrombosis to a varying extent may occur, by which the vein is changed to a hard cord. In this condition the local and general sjnnptoms vary according to the degree and charac- ter of the concomitant inflammation. Should the venous dilatation subsist for a long time under the influence of a persistent cause, serous transudation into the connective tissue at last occurs, which by long continuance leads to induration and favors the occurrence of accidental inflamma- tion. The mucous membranes lying within the range of such veins are subject to chronic catarrh. Of all the various venous areas within the body, that of the vena cava superior is much less frequently affected with dilata- tion than that of the vena cava inferior. For the most part in it the dilatation begins and is greatest close to the heart, gradually decreasing towards the periphery. The jugular veins in such cases are seen in the neck like round cords, the external jugu- lars being as thick as a finger, while the internal jugulars may reach the size of an infant's arm ; they are more or less tortu- ous, often visible quite up to the cranium, and becoming turgid at each expiration or paroxysm of coughing. The bulb of the internal jugular vein is usually specially visible just before and behind the origin of the sterno-cleido-mastoid muscle. The venous swelling is usually better marked on the right than on the left side, but not always. When the dilatation is consider- able, the venous valves become insufficient, so that regurgitation is caused by the expiratory movements or by the cardiac con- tractions. The venous pulsations can then be recognized, some- VOL. VI.-32 498 QUINCKE.—DISEASES OF THE VEINS. times as presystolic, synchronous with the auricular pulsation, at others as systolic, synchronous with the ventricular contrac- tion, and at still others both phases may be recognized in the form of an anadicrotic elevation. Which of these forms of pulsa- tion is most evident depends upon the intensity of the contractile power of the individual cavities of the heart, on the presence of tricuspid insufficience, or on the momentary degree of tension within the vein. Sometimes, when the venous valves are insuf- ficient, a stenotic murmur is audible synchronous with the venous pulse or with forcible expiration ; a thrill is often also perceptible. Those veins which are surrounded by denser tissues, such as the subclavian veins and their branches, are less frequently dilated than the veins of the neck, and their valves are less commonly insufficient. The causes of this dilatation are : defective empty- ing of the right ventricle, diminution of the negative pressure within the thorax by disease of the lungs, etc., tumors which compress the anonymous veins, or, finally, the long continuance of violent paroxysms of coughing. The thyroideal veins are often dilated to cords the size of a finger (their coats often concomitantly hypertrophied) in the various forms of struma. This is most remarkable in struma vasculosa, in which there is a kind of hypertrophy of all the vessels of the thyroid gland; it is less evident, though always considerable, in struma hyperplastica, in which the vessels become enlarged from the persistent increase of the blood flovr through the thyroid gland. In the face, dilatation of the smaller veins of the cheek and nose are seen in disease of the heart and lungs, in alcoholism us, and in acne rosacea. Small varices occur on the eyelids, the lips, and the tongue, as well as in the mucous membrane of the fauces in chronic catarrh. The meningeal veins are dilated and tortuous in general venous congestion and in atrophy of the brain {ex vacuo). Meschede' has recorded a saccular and laterally situated varix of the superior longitudinal sinus, with a corresponding atrophy of the skull. 1 Virch. Arch. Bd. 57. S. 525. 1873. DILATATION. —SYMPTOMS. 499 Venous dilatation in the upper extremities is observed when the main trunks are compressed by a tumor ; in rare cases it is congenital. Dilatation of the veins within the area of the vena cava in- ferior are more frequent and more important. On the trunk of this vein and the first large branches given off, the hepatic and renal veins, the dilatation is usually caused by disease of the heart or lungs ; within these venous areas it generally extends even into the capillaries, and results in serous soaking, with induration of the kidneys and liver ; in the case of the latter organ the long continuance of the pressure of the dilated capil- laries leads indeed to atrophy of the hepatic parenchyma, and contraction of the organ (atrophic nutmeg-liver). Of all the veins within the area of the inferior cava those most frequently dilated are the veins of the lower extremities, especially of the legs; they are also usually varicose. They give us by far the best opportunity of studying the pathology of venous dilatation generally. Occupations necessitating con- tinuous standing (less frequently those requiring walking), the pressure of the pregnant uterus, of faecal masses or of other tumors upon the vena cava, the pressure of tumors or of garters on the extremities, are its most frequent causes. The great cuticular trunks of the two saphenous veins are often seen as thick cords; should the dilatation affect these trunks alone or principally, the inconvenience may be but trifling'. But the more numerous are the branches implicated, so much the greater is the tendency to oedema, cuticular inflam- mations (eczema, erysipelas, boils), and to sclerosis of the subcu- ticular connective tissue—conditions which, in their turn, favor the progress of the venous dilatation. Ulcers are readily caused, but heal with difficulty, and may by erosion of a vein give rise to considerable hemorrhage. Sometimes concomitantly with the cuticular veins, at others independently, the deep-lying veins of the leg are also dilated and varicose; the patients have then a sensation of weight, fatigue, spasmodic tension, and numbness in the leg when they walk or stand. Sometimes a deep-seated, diffuse hard swelling can be felt. Dilatation of the veins of the spermatic cord, varicocele, also 500 QUINCKE.—DISEASES OF THE VEINS. belongs to the domain of surgery. This is a very frequent ail- ment, almost exclusively occurring on the left side, apparently because the current of the venous blood is liable to be ob- structed by the pressure of the sigmoid flexure of the colon, and because it terminates in the renal vein, and not directly in the vena cava, as the right spermatic vein does. The varicocele is accompanied by dragging pains in the testicle and cord, and sometimes with involuntary emissions ; it may ultimately lead to atrophy of the testicle. The cuticular veins of the abdominal walls are somewhat dilated whenever the abdomen is distended from any cause (such as gravidity, ascites, etc.). The dilatation is very considerable whenever these veins are involved in promoting a collateral circulation (through the epigastric, the mammary, the intercostal, the azygos, and the hemiazygos veins) in cases of compression of the inferior cava or the portal vein. In the case just referred to, the small cuticular veins around the navel are often dilated as a vascular corona (caput medusae), by the blood conveyed to them from the portal vein by the still pervious umbilical vein, or by the parumbilical vein. In such a case the portal vein is dilated up to the contracted part (of its trunk or of its branches within the liver, as in cirrhosis). The veins of the pelvic organs communicate so freely with each other by means of plexuses and anastomoses that their dila- tation will be more conveniently dealt with under the head of dilatation of the hemorrhoidal veins, as this most frequently is the point of origin of venous dilatation within the pelvis. The veins of the female sexual organs are, however, not unfrequent- ly independently dilated in advanced life, as the result of re- peated pregnancies or of inflammatory conditions of the uterus and its connections. Treatment. The treatment of venous dilatation mostly belongs to the department of surgery, but particular attention must be paid to the causal phenomena (such as cardiac and pulmonary disease, compressing tumors, constipation, etc.). LATATION OF THE HEMORRHOIDAL VEINS. 501 When the dilated veins are still pervious, as in the extremities or in the scrotum, then we must seek to support their walls ex- ternally by enveloping the parts affected in simple or elastic band- ages, and to restore their tone by cold bathing and friction. The effort has also been made to attain this by injecting ergotine into the surrounding cellular tissue; yet, as has been already mentioned when speaking of a similar treatment of aneu- rism, the results observed are more probably produced by the influence of compression and inflammatory irritation. As in aneurism, extreme measures have been resorted to, and thrombosis and obliteration of the vessel by coagula have been sought to be produced by injec- tions, electro-puncture, etc. ; indeed, quite recently, several inches of a dilated saphenous vein have been cut out. The treatment recently recommended by Ravoth is of great theoretical as well as practical interest; he employs central compression of the dilated venous trunks by means of a ball of feathers (hernial truss). A priori, one would rather expect a further increase of the dilatation from such an obstruction to the onward circula- tion. R. explains the result as arising from a quickening of the circulation through the veins (?) and a partial relief to the tension of their walls. (It seems more prob- able that, as the result of the compression, collateral veins are gradually dilated, and, as these continue to convey a large part of the blood even after the removal of the compress, the blood-pressure is permanently diminished in the veins originally dilated.) According to C. O. Weber, Colles had previously employed a similar treatment. In DILATATION OF THE HEMORRHOIDAL VEINS, The uniformly cylindrical form of dilatation is combined with a varicose condition. The plexus of veins lying in the submu- cous tissue of the lower part of the rectum, and in the adjoining subcutaneous connective tissue, are those chiefly affected in this form of dilatation ; but it is also very common for the venous radicles in the mucous membrane itself, the perirectal plexus, and the adjoining venous plexuses of the bladder, uterus, vagina, and the sacral canal, to be also implicated in this dila- tation. Isolated, strongly distended varices bulge outwards the mu- cous membrane or the delicate skin of the anal margin in a saccular form ; in other parts the pressure of several distended 502 QUINCKE.—DISEASES OF THE VEINS. veins upon one another produces local absorption of the venous coats, and a system of communicating blood sacs is thus ori- ginated. This venous dilatation does not leave unchanged either the mucous membrane or the submucous tissue; capillary venous hyperaemia, serous transudation, hyperplasia of the connective tissue, and catarrhal swelling of the mucous membrane are associated with it, while in other places these tissues atrophy under the influence of the pressure of the varices. The natural rugosities of the rectal mucous membrane become permanently thickened and inflamed, polypous growths are formed and asso- ciated with the more or less pedunculated tumors produced by the varices. These hemorrhoidal tumors range from the size of a pea to that of a pigeon's egg, and vary exceedingly in volume, according to the amount of venous turgescence; sometimes they are small, relaxed, and corrugated, at others large, turgid, and shining. According as they are situated within or without the anal margin, they are termed internal or external hemorrhoids. Like all other venous dilatations, these also undergo many secondary changes and degenerations ; and they are, from their situation, specially exposed to mechanical injuries of the most manifold character. The consequences of these are, rupture with hemorrhage either external or into the connective tissue, inflam- mation of the coats of the vein, or thrombosis of a hemorrhoidal tumor resulting in obliteration or suppuration. The submucous and perirectal connective tissue is also liable to become sclerosed or purulent as the result of inflammation, and the inflamed catarrhal mucous membrane of the rectum, or the skin sur- rounding the anus, may be eroded and ulcerated. Prolapsed varices and rugosities of the mucous membrane may be strangu- lated and necrosed by the pressure of the sphincter. Etiology. The most common cause of dilatation of the hemorrhoidal veins is obstruction to the onward flow of the blood, especially by habitual accumulation of faeces in the rectum, and also by DILATATION OF THE HEMORRHOIDAL VEINS. 503 other tumors within the true pelvis; since the larger portion of the venous blood from the rectum is conveyed to the portal vein, by means of the superior hemorrhoidal vein, any perma- nent or repeated turgescence of the portal system, from conges- tion or frequent and copious meals, contributes to the production of hemorrhoids (consequently also any disease of the liver, such as hyperaemia or cirrhosis) ; disease of the heart and lungs may also act similarly through the vena cava itself or inter- mediately through the portal system. Abdominal tumors, the pregnant uterus, or great accumulation of fat in the omen- tum may also give rise to portal congestion. As in other mucous membranes, so also in that of the rec- tum, persistent chronic catarrh seems to favor the production of venous dilatation. Dilatation of the rectal veins is an extremely frequent condi- tion in all those who suffer from chronic constipation as the result of their diet or habitual occupation, consequently in all those who live freely and take much vegetable food, who lead sedentary lives and take little exercise, such as clerks and simi- lar officials. Much horse exercise also disposes to the formation of hemorrhoids (partly from the constipation thus induced, partly from the direct irritation of the part). From the manifold character of the causes just narrated, it is easy to see that in individual cases several of these may often occur together, and that their effects may be cumulative, indeed that in the production of hemorrhoids, catarrh of the rectum and constipation may prove a circulus vitiosus, the individual elements of which may serve mutually to induce and aggravate each other. It is probable that the hindrance to the respiratory move- ments induced by constipation, accumulation of fat within the abdomen, and sedentary habits, etc., may be an important adju- vant cause in the production of venous dilatation, since the pres- sure variations induced by the respiratory movements, both in the abdominal and in the thoracic cavities, are assuredly an im- portant means of promoting the circulation within the abdomen. Even when all the appropriate conditions are present, they by no means always give rise to dilatation of the hemorrhoidal 504 QUINCKE.—DISEASES OF THE VEINS. veins, and still less frequently to its obvious (objective) occur- rence. Predisposition, probably often hereditary, plays in regard to this a most important part. In middle life and in the male sex this affection is most com- mon. It is very rare in childhood. Symptoms. A moderate dilatation of the hemorrhoidal veins often gives rise during life to no symptoms whatever ; it is either altogether unnoticed, or the individual affected may accidentally discover by touching his anus that small tumors exist there. Even when subjective disturbances are present, these only occur periodically, when with or without any evident cause (most frequently constipation) the veins become congested, and turgescence, hyperaemia, or even inflammation of the adjacent parts may occur. A sensation of burning, itching, and fulness in the anus is felt, especially when it is irritated by the passage of hard faecal masses, and the sphincter thus excited in a reflex manner to more vigorous contraction. Objective examination brings to light in the neigh- borhood of the anus more or less tense elastic tumors, peduncu- lated or with broad bases, which, according to the thickness of the skin covering them, are either of a bluish-black or reddish- white color. When submucous varices are present, these may be felt by the finger, passed through the anus, as tumors the size of a straw- berry or grape ; more rarely these are prolapsed, and by strangu- lation by the sphincter become turgid and very painful. The burning and itching are greater the more the surround- ing skin becomes erythematous, inflamed, or excoriated ; when catarrh of the rectum is simultaneously present, this is accom- panied by violent tenesmus and the escape of a glairy mucus, which by and by becomes purulent. The anus is contracted by the tumefied mucous membrane, and the latter is not unfre- quently prolapsed. The pain in the anus is intense, stinging;, and radiating towards the bladder and sacral region. Fissures of DILATATION OF THE HEMORRHOIDAL VEINS. 505 the mucous membrane in the neighborhood of the sphincter iire specially painful. All these sufferings are most severe during defecation, walk- ing, standing, or sitting, but are lessened by the recumbent posture. Should the local inflammation be intense, fever, loss of appe- tite, and disturbance of the general health may occur. Blood frequently escapes during defecation, and this either conies from the capillaries and excoriations of the inflamed mu- cous membrane, or—more rarely—from a ruptured varix, and in the latter case it may escape externally. The effused blood in such cases is recent, not mixed with the faeces, and unaltered by the gastric juice. Usually the hemorrhage is trifling, and caused by the passage of the faeces. Sometimes after a somewhat copious hemorrhage —such as a few tablespoonfuls—there occurs a remission of all the sufferings, from diminution of the swelling of the veins and of the mucous membrane. Hemorrhoidal hemorrhage is very rarely injurious from its amount, and only so in weakly individ- uals. Moreover, it seldom occurs in those who are anaemic, and therefore it commonly ceases in advanced life. These periodical attacks, the so-called fits of the piles, occur in greater or less violence and alternate with long periods, during which either no disturbances at all or only very trifling ones occur. However troublesome the attacks may be, they are seldom dangerous. When the inflammation is acute, or when a nodule is strangulated, thrombosis may occur. As the result of this the varix may be obliterated, or inflammation may occur in its neighborhood, and this may lead to suppuration, to proctitic or periproctitic abscesses, and the formation of fistula; in severe cases purulent phlebitis, with pyaemia and metastatic abscesses, may occur, especially when the tumors have prolapsed, and have become strangulated and gangrenous. As already mentioned, the other venous plexuses within the pelvis are not unfrequently implicated in the dilatation affecting the hemorrhoidal veins. When the vesical and prostatic plexuses are affected, there is present a frequent desire to micturate, and 506 QUINCKE.—DISEASES OF THE VEINS. pain in the act of micturition. The mucous membrane of the bladder is liable to catarrh, and blood is often mixed with the urine. Dilatation of the sacral plexus is revealed by pain and a feel- ing of weight in the sacral region; when the communicating plexus of the spinal canal is affected, it may, by compressing the roots of the nerves, give rise to sensations of weight, numb- ness, formication, and pain in the lower extremities, or even in the lumbar region, so as to simulate sciatica, or a lesion of the cord itself. Catarrhal affections of the female genital organs are kept up by dilatation of the veins, and tumefaction and inflammation of the uterus itself are thereby favored. Menstruation is often copious ; it however serves to unload the veins at regular intervals, and thus it happens that dilatation of the hemorrhoidal veins is first fully developed in women after the cessation of the menses. On the other hand, the hemorrhoidal veins often become turgid coetaneously with the uterine menstrual flux. When numerous concomitant phenomena are associated with the results of simple dilatation of the veins, the totality of the symptoms is often made to appear extremely complex by the presence of other morbid phenomena, which are either them- selves the prime agents in the production of this venous dilata- tion, or which originate with it in a common cause. Thus we see diseases of the heart or lungs give rise concomitantly to the most manifold symptoms of liver disease, and of anomalies in the digestive and nutritive processes, with all their various con- sequences. And thus it is easily explicable why in earlier times such extravagant importance was attached to the presence of hemorrhoids, one symptom arising from very various conditions having been regarded as the essence of the disease. The diagnosis is simple, as soon as we examine the patient ob- jectively ; but from the subjective phenomena alone this affection might easily be mistaken for syphilis, carcinoma, or a simple polyp of the rectum. For the treatment it is further of impor- tance to determine what are the predisposing and proximate causes. The general prognosis depends upon these, for actual danger DILATATION OF THE HEMORRHOIDAL VEINS. 507 can only exceptionally arise from a purely local affection. A perfect cure is, however, very rare. Treatment. The treatment of dilatation of the hemorrhoidal veins must be directed against its causes, such as diseases of the liver and heart, and disturbances of the digestive process, etc. Even where constipation has not been a proximate cause of the disease, regulation of the bowels is nevertheless an important means of diminishing present and preventing future troubles. The food must, therefore, be moderate, unirritating, leaving but little faecal refuse, and its composition must as far as possible be of such a nature as to favor secretion and the peristaltic movement of the intestines (such as fruits, certain vegetables, etc.); the regulated use of cold water and regular exercise also assist in producing the same end. Often enough such a system of diet is sufficient to reduce the trouble to a minimum ; when this is not the case, mild saline laxatives, mineral waters, or rhubarb, may be employed as adjuvants. Aloes or colocynth in small doses are also perfectly appli- cable, either with or without the addition of extract of belladonna. The curative use of Marienbad, Kissingen, and other mineral waters, of grapes, and the juices of various herbs, is not only useful symptomatically, but often fulfils causal indications. Cold washing, clysters, and sitz-baths are also important remedies to keep the rectum and anus free and clean, and to prevent inflammation. Special attention must be paid to the regulation of the diet and bowels during an attack of piles ; clysters and the internal use of castor-oil are to be employed to keep the rectum free from faecal accumulation, and to disembarrass the circulation; the horizontal position must be preserved, and the covering must be light and cool. Local inflammations are to be treated by cool sitz-baths and fomentations, or, if more severe, leeches may be applied. Ointments, suppositories, or injections of tannin, salts of lead, etc., are useful in more trifling irritation, and in the 508 QUINCKE.—DISEASES OF THE VEINS. concomitant erythema and rectal catarrh. Narcotics internally and locally are indispensable when the pain is violent. A moderate amount of hemorrhage often gives relief and re- quires no treatment; even should it be more considerable, it still is usually easily restrained by the application of cold fomentations, clysters, or sitz-baths. At other times astringent fluids (liquor ferri perchloridi), and, in extreme cases, plugging the rectum, or the hot iron may be necessary. Thrombosed nodules must as much as possible be guarded from violence so that they may become organized. Purulent inflammations and their results are to be treated upon general principles. Large external varices may be removed by the hot iron. Narrowing and Obliteration of the Veins. A uniform narrowing of the veins over any considerable ex- tent is of rare occurrence, and happens in parts which are be- coming atrophied, as the result of the diminution of the blood stream. J. Gay' has described cases of what he calls " hypovenosity,1' in which there is a diminution in the size and number of the veins in the area of the saphena, and in which (probably as the result of the pressure of the collaterally dilated deep veins) atrophy and fatty degeneration of the muscles are developed. The limb ig wasted, but tense, sinewy, and painful; movement is difficult, and the skin dark- colored. Improvement of the nutrition by exercise, friction, and warm baths are said to be useful. Local narrowing or occlusion of the veins is of much more common occurrence. Apart from thrombosis, presently to be referred to, which is the most common cause of these narrowings, they are produced by the pressure exerted from without on the veins by tumors, organs which are inflammatorily swollen, or by cicatrices. Concomitant chronic inflammation of the walls and clot-formation often assist in producing this narrowing. This 1 Lancet. Nov. 1871. RUPTURE AND WOUNDS. 509 condition may lead at last to complete occlusion of the vein ; the walls of the vein, pressed one upon the other, grow together and are changed into a simple cord of connective tissue. The area of the radicles of the narrowed vein exhibit all the signs of venous congestion (in so far as this is not efficiently relieved by the establishment of collateral dilatation): such as dilatation of its affluent branches, down to the capillaries, cyanotic discoloration, a diminution of temperature, serous transudation, etc.,—phenomena which will be more particularly referred to when speaking of thrombosis, and which are all the more prominent, the more rapidly the narrowing is brought about, and the shorter the time afforded for the development of a collateral circulation.1 Rupture and Wounds of Veins. Rupture or wounds of veins may be produced— 1. Traumatically, by cutting instruments, accidentally or operatively (venesection), usually only in superficial veins ; also by crushing or tearing, by falls from a considerable height; or the large thoracic or abdominal veins may be ruptured when the body is driven over by any carriage, or the veins of the extremi- ties may be torn across by violent muscular exertion or by direct blows. Coester' saw perforation of the vena cava inferior by a sharp-pointed piece of bone which had caught in a diverticulum of the oesophagus. Death resulted from hemorrhage into the right pleural cavity and the stomach. 2. By increased pressure within a vein, such as exists in cases of congestion of a central origin, or when a communication with an artery has been made. Thus the pulmonary veins are some- times ruptured in cases of disease of the mitral valve. 3. By disease of the venous coats. This, however, can but seldom be the cause of rupture, since inflammation usually very 1 Vide Destord, Des Tumeurs cmcereuses du mediastin avec compression ou oolite^ ration de la veine cave supcrieure. These de Paris, 1866. 2 Berliner klin. Wochenschr. 1870. No. 43. 510 QUINCKE.—DISEASES OF THE VEINS. early leads to coagulation of the blood. Atrophy of the walls, such as occurs in dilatation of the veins, or fatty degeneration (as in one case of rupture of the portal vein related by Frerichsl) is more likely to lead to rupture. 4. By ulcerative destruction of the venous coats, which occurs in suppurative phlebitis of a primary or secondary charac- ter (as, for instance, in deeply penetrating ulcerations). Rupture may also result from the pressure of an adjoining tumor, for example, an aneurism, or by the vein becoming implicated in its growth (as in the case of a carcinoma). Rupture occurs, on the whole, more frequently in veins than in arteries, since from the thinness of their walls and the trifling degree of elasticity they possess, the former are less capable of resistance than the latter. Symptoms.—In wounds or lacerations of the peripheral veins, when the blood stream can readily find its way through collateral vessels and the blood pressure is thus not very great, coagulation of the blood readily occurs at the part wounded, which is thus closed. At other times the blood flows externally or into the adjacent cellular tissue until the blood pressure within the veins is diminished, or is exceeded by that external to them. The blood effused into the cellular tissue causes swelling and pain, sometimes even inflammation of the part affected, or it may be reabsorbed without the occurrence of any important local or general disturbance. Should one of the large veins in the chest or belly be torn, the hemorrhage takes place into loose cellular tissue or into one of the serous cavities, and the patient dies with all the symptoms of internal hemorrhage in a few hours, rarely surviving for a few days. Sometimes such patients have had a sensation as if some- thing within them had been torn. Occasionally the blood can be detected within the serous cavity before death. Instead of or along with the escape of blood from the veins, foreign matters may gain an entrance into the injured vein ; in suppurative destruction of the venous coats, pus, or ichor, or cancer-juice may get into the veins, and thus lead to septicaemia, 1 Leberkrankheiten. II. S. 382. New Syd. Soe. Transl. II. p. 404. RUPTURE AND WOUNDS. 511 embolic inflammations, or the development of secondary cancers, provided the venous lumen has not been previously occluded by a coagulum. The prognosis depends upon the position and size of the vein injured. In rupture of any of the large veins within the cavities of the body, treatment is of no avail. When the position of the vessel is such as to permit it, the part ruptured must be elevated, local compression made use of, and cold applied. The introduction of foreign matter into the veins of inflamed parts will be best prevented by diminishing the tension of the inflamed part and promoting the flow of the pus externally (position, incisions). DISEASES OF THE LYMPHATICS. Vide the handbooks of pathological anatomy by Cruveilhier, Forster, Rokitansky, etc.; also the handbooks of special pathology and of diseases of the vascular system by Wunderlich, Lebert, Duchek. Andral, Arch. gim. de med. 1824. Vol. 6. p. 502.—Assalini, Essai medical sur les vaisseaux lymphatiques. Turin. 1787.—Attenhofer, Lymphatologie. Wien. 1808. — Cohn, Embolische Gefasskrankheiten. S. 110 and 659.—Cruikshauk u. Mascagni, Gesch. und Beschreibung d. Saugadern, 1789.—H. Emminghaus, Physiologisches und Pathologisches iiber die Absonderung und Bewegung der Lymphe. Arch. d. Heilk. 1874. Bd. 15.—Genersich, Lesser, Pasehutin, Ernming- hatm, Ueber Lymphabsonderung in den Ber. iiber die Arb. d. physiol. Instituts zu Leipzig. 1870-73.— Goodlad, A practical essay on the diseases of the vessels and glands of the absorbent system. London, 1814.—Rayer, Dictionn. de medec. Art. Hydropisie.—Salmade, Precis d'observations sur les maladies de la lymphe. Paris. 1803.—Soemmering, De morb. vasor. absorbent. Frankf. 1795.— van Swieten, Comment. IV. p. 116. — Teichmann, Das Saugadersystem.— Velpeau, Arch. gen. 1835. Vol. VIII. pp. 129 and 308 ; 1836. Vol. X. p. 5.—0. Weber, in Billroth-Pitha's Handb. d. Chirurgie. II. 2. S. 63. 1865.— Wrisberg, De syst. vas. abs. morbos excit. et san. comment, soc. reg. Gotting. 1789. Bd. IX. Diseases of the lymphatics, just as much as those of the blood-vessels, are most intimately connected in various ways with the most diverse organic diseases ; perhaps this connection is even more close, since the capillary lymphatics, according to many authors, are in open communication with the spaces of the tissues. For evident reasons, we have been obliged in the follow- ing chapter to omit all consideration of the diseases of these lymphatic capillaries, as was also done in regard to the blood capillaries. It will readily be seen, from the contents of the following paragraphs, that our knowledge of the pathological conditions of the lymphatic vessels is as yet very imperfect. The trans- LYMPHANGITIS.—BIBLIOGRAPHY. 513 parency of their contents, its capacity for imbibition, the thinness of the walls, the trifling rate of movement, and low degree of tension of the lymph-stream, are all to be regarded as phenom- ena which obstruct any attempt at anatomical investigation of the subject; indeed, any accurate knowledge of the anatomical and physiological relations of the lymphatic system dates, for the most part, from quite recent times. It is possible that many obscure pathological conditions owe their origin to disturbances of the lymph-stream ; even van Swieten referred the occurrence of dropsy to this, partly directly and partly indirectly, by means of the venous blood-stream, and, according to our present knowledge, it is not improbable that certain cases of ascites, of pleuritic effusion, and of hydro- cephalus, not connected with obstruction to the circulation of the blood, may depend upon embarrassment of the lymph- stream. The dependence of elephantiasis upon disease of the lymphatic vessels is to be regarded as almost certainly proved, as will be presently shown. Inflammation and simple thrombosis of the lymphatics can- not as yet, on the basis of our present knowledge, be clearly separated from one another, and must, therefore, be treated of together. Inflammation and Thrombosis of the Lymphatics. Lymphangitis, Angioleucitis. Allard, De Tinflammation des vaisseaux absorbens. Paris. 1824.—Bouvel-Ronciere, Les lymphangites primitives de Rio de Janeiro. Arch, de med. navale. Mai, 1873. p. 355.—Breschet, Du syst. lymphat. These de Concours. 1836.—Browne Cheston, Philos. Transactions. 1780. Vol. LXX. p. 323. — Cooper, Med. records and researches selected from the papers of a private med. assoc. Lond. 1798. I. p. 28.—Duplay, Arch. gen. 1835. Vol. VII. p. 10. De la suppuration des vaisseaux lymph, de Tuterus.—Fetzer, Ein Fall von eigenthiiml. Erkrankung der Lymphgefasse. Arch. f. physiol. Heilk. 1849. Bd. VIII. S. 128.—Kiwischr Klin. Vortrage. I. S. 632.—Leopold, Die Lymphgefasse des normalen nicht schwangern Uterus. Arch. f. Gyntekol. Bd. VI. S. 1. 1873— Ludwig, Wien. med. Jahrb. 1863. XLX. Z.—Ojyolzer, Allg. Wiener med. Zeitung. 1861. No. 19. — TonneU, Arch. gen. 1830. Vol. XXII. p. 354.— Turner, Edinb. Med. Journ. VOL. VI.—33 514 QUINCKE.—DISEASES OF THE LYMPHATICS. 1859, May (2 cases of occlusion of the thoracic duct by aneurisms).— Yirclww, Arch. Bd. XXIII. 1862. S. 415.— 0. Weber. In Billroth-Pitha's Chirurgie. II. 2. S. 63.— Weitenweber, Beitr. Bd. IV. H. 2. —/. Worms, De rinflammation du canal thoracique. Gaz. Hebdom. 1859. p. 280. Anatomy. Inflammation of the lymph-vessels, as of the veins, seems chiefly to affect the external portion of their coats. The adven- titia and the surrounding connective tissue appear injected, swollen, cloudy, and infiltrated with cells ; the intima is opaque, uneven, and stripped of its epithelium. The lymphatic glands connected with the part affected are swollen or inflamed. The inflamed lymph-vessels are often dilated, partly from relaxation of their walls, partly because the onward flow of their contents is hindered. Instead of a normal, transparent lymph, they con- tain a thick, opaque fluid, full of cells, which may even be puri- form, and may coagulate, and thus occlude the vessel; }^et such coagula are rarer, not so readily formed, and less firm than the thrombi in the blood-vessels. They are white, pale, red, or yellowish, like pus, and exhibit under the microscope mainly a finely granular mass with lymph corpuscles sparingly scattered through it (0. Weber). Such thrombi are most apt to be formed in the immediate neighborhood of the valves. The results of the inflammation, as well as the further changes in the thrombi, are precisely analogous to those occurring in the blood-vessels in similar circumstances. When the inflammation is trifling, the new-formed cells disintegrate, and the exudation is absorbed; but relaxation and dilatation of the lymphatic vessels is a very frequent result. In other cases the inflammation leads to hyper- plasia of the connective tissue ; thickening of the wall of the vessel, sclerosis of the surrounding connective tissue, and narrow- ing or obliteration of the lymph-vessel are the consequences. Finally, the inflammation of the lymphatics may lead to suppura- tion of the walls of the vessels and of the surrounding connective tissue. It is characteristic of all forms of inflammation of the lymphatic vessels that the cellular tissue is wont to be implicated in a very much greater degree and over a greater extent than in LYMPHANGITIS.—ANATOMY. 515 inflammations of the blood-vessels ; it is possible that this may depend upon the comparative thinness of the walls of the lymph- vessels and their less distinctly defined separation from the tissue spaces. The coagulated contents of the lymph-vessels undergoes changes analogous to those of thrombi within the blood-vessels ; it may be absorbed, may break down into pus, may become organized or calcified. Sometimes we find the contents of the lymph-vessels coagulated, opaque, rich in cells, or even purulent, without there being any very evident disease of the coats of the vessel; in such cases the contents of the lymphatics seem first of all to be altered by the entrance of foreign matter, or by the primary disease of the organs in which these vessels originate, and this alteration of the contents seems to give rise to a second- ary affection of the coats of the vessel. From the narrowness of the vascular lumen, only fluids, or very minute bodies suspended in them, can be convej^ed along with the lymph-stream ; very rarely are thrombi swept along with the current, as happens in the blood-vessels. Such solid particles seem not to pass beyond the nearest lymphatic gland ; yet the inflammation of the lymphatics may be propagated beyond these glands, the irritating matter being conveyed beyond them, either in solution or in the interior of the lymph cells. Moreover, I may remark that our knowledge of the anatomy of inflammation of the lymphatic vessels is extremely defective, and this depends partly on the fact of the inconstancy of the course of even large lymphatic trunks, as well as on the thinness of the walls, and narrowness of the calibre of these vessels, and partly because this inflammation seldom occurs by itself, but is usually secondary and accompanied by implication of the sur- rounding tissues. What has just been said of the larger lymphatic trunks is even more applicable to the lesser lymph vessels, because the variations in regard to their distribution and normal anatomical structure are even more manifold. In parenchymatous inflam- mations these are undoubtedly very often coetaneously diseased, and convey the products of morbid tissue change. The proof of this conveyance of morbid products is to be found in the frequent occurrence of consecutive disease of the lymphatic glands, in 516 QUINCKE.—DISEASES OF THE LYMPHATICS. which these products seem to accumulate, whilst the lymphatic vessels, through which these products pass often for considerable distances, are not themselves inflamed. Etiology. Lymphangitis occurs very rarely spontaneously, but is almost always secondary to disease of the area in which the radicles of the lymphatic vessel affected originate. The products of the morbid tissue change, which are conveyed by the lymphatics, appear to be the active agents in inducing this form of disease. It appears to depend upon the nature of these products, as well as upon the nature of the inflammatory process itself, whether the lymphatics are themselves implicated in this morbid process or not; possibly this may also partly depend upon whether the lymphatic radicles in the part primarily diseased remain open or are closed by clots or pressure. Sometimes an independent lymphangitis is simulated, when the primary disease from its trifling character remains unnoted. This is specially the case in slight external injuries, pricks, scratches, and abrasions of the skin, which lead to lymphangitis, not from their own intrinsic character, but by giving entrance to injurious matters, such as decomposing or putrid organic mat- ters, and the secretions and parenchymatous fluids of inflamed organs ; for this reason anatomists and medical men are specially apt to be affected hy lymphangitis. While the flow of blood and of the inflammatory secretions readily cleanse the surfaces of large gaping wounds from any foreign substances which may ad- here to them, this is not the case in trifling pricks and scratches ; and to this source of danger we must add the slight attention paid to such injuries. The local inflammation is often slight, or may be entirely absent, while the emerging lymphatics may be actively inflamed. Lymphangitis has also been observed to follow the stings of insects, the bites of our indigenous (but little hurtful) poisonous snakes, etc. Further, we see this disease originate in the most various parts of the body as the result of inflammation, suppuration, or the formation of ichor in the connective tissue, whether these pro- LYMPHANGITIS.—SYMPTOMS. 517 cesses have actually occurred in the area of the radicles of the lymph vessels affected, or whether the disease has spread by contiguity from the neighboring tissues. Lymphangitis is of very frequent occurrence when the pelvic connective tissue is in- flamed during childbed. Symptoms. The clinical phenomena attending inflammation of the lym- phatic vessels are best known as they occur within the domain of surgery in external parts, particularly the extremities, and most frequently as the result of poisonous wounds. But a few hours after the receipt of such a wound, the superficial lymphatics of the skin appear as pale red lines ; these sometimes form an anastomosing network, and run together; they are painful on pressure, and may be felt as hard, knotted cords, which are not usually sharply limited. These lines and cords cannot always be traced directly to the injured part. This part itself, as well as the whole area from which the inflamed lymphatics arise, is swollen, by reason of the defective removal of the lymph, and this swelling is greater, the more extensive the lymphangitis is, and the fewer collateral routes therefore remain open. Should the deep-tying lymphatics be inflamed, the redness may be absent, or only punctiformly indicated ; the pain is violent and less circumscribed, the swelling considerable, and generally diffuse. The corresponding lymphatic glands are invariably concomi- tantly affected, painful, and swollen, often in several positions simultaneously (as, for example, the cubital and axillary glands); between the painful glands and the inflamed lymphatic ves- sels, there is not unfrequently a part of the latter which is apparently quite unaffected. Fever is usually present; often it is of considerable intensity, and commences with a rigor. Should the disease run a favor- able course, it commences to abate in from a few days to a week ; the local symptoms disappear (the oedema being the last to do so), and a cure follows. At other times, suppuration—originating either in the con- CIS QUINCKE.—DISEASES OF THE LYMPHATICS. nective tissue, or in the lymphatics themselves—extends along the inflamed vessels ; in these cases a cure may at last result, accompanied by cicatrization and destruction of the vessels, or the fever may assume a typhoid character, and death from pyaemia may follow. The lymphatic glands are generally implicated in the changes which take place in the afferent vessels, but they more readily suppurate than the latter. Should any part of the inflamed lymphatics become destroyed or narrowed, the affected tissues sometimes remain oedematous, and this subsequently leads to sclerosis and permanent hypertrophy of the connective tissue, which may be either diffuse or in isolated lumps or masses. Many cases of elephantiasis, both indigenous and tropical, seem to owe their origin to repeated inflammations of the lym- phatics (in connection with erysipelas and other skin affections. On the other hand, Wernher assumes that the lymphatics are simply dilated. Vide postea, p. 528) Many cases of puerperal phlegmasia alba dolens, of sclerema (hidebound disease of new-born children), and of epidemic angina parotidea, have been referred to inflammation of the lymphatic vessels, but without any sufficient proof having been given that this has been really the actual and primary cause of the disease. Bouvel-Ronciere describes an idiopathic lymphangitis malariosa (popularly known as the Rio-de-Janeiro erysipelas), which affects the superficial or deep lym- phatics of the whole body, often in several places simultaneously, and in which the surrounding connective tissue is also implicated. Should the disease be limited, convalescence occurs in a few days; in severer cases, those affected die from adynamia or from suppuration. The treatment consists mainly in the use of qui- nine, besides local applications. The Prognosis of lymphangitis varies with the extent of the disease and the nature of its proximate cause. Sometimes, even when the disease is of but limited extent, the general symptoms are very severe, and the disease terminates unfavorably after assuming the form of a septic fever; this is ascribed to the virulence of the infecting substance, of which we have no more accurate knowledge, while its very existence is only proved by the severity of the infection. In general, the prognosis is all the more favorable the nearer the LYMPHANGITIS.—TREATMENT. 519 periphery the part affected lies, since the interpolated glands often set a limit to the centripetal progress of the inflammation. The Treatment must be chiefly directed against the proximate cause ; therefore, recent wounds must be dilated, cleansed, cauterized, or disin- fected by fluid or diffluent remedies (such as acetic acid, caustic potash, chloride of zinc, carbolic acid, etc.), and afterwards care- fully treated like other primary inflammations, according to the fundamental principles of surgery. The diseased part must be kept at rest. Leeches are but seldom required, and only when great pain is present over a limited area. Locally, cold is to be applied at first, and subsequently poultices and tepid baths. Envelopment in raw cotton and inunction with blue ointment have also been much recommended. Abscesses must be opened as early as possible. Internally we may employ vegetable and mineral acids, quinine, alcohol, and other remedies usually prescribed in infec- tive processes. Residuary oedema and indurations are to be treated by appropriate position of the part, compression, warm baths, painting with iodine, oily inunctions, and methodic sham- pooing. Passive movements, the alternate flexion and extension of the part, seems also a rational mode of treatment, now that (renersieh, Lesser, and Paschutin have taught us how very much the flow of the lymph is favored by such manipulations. Inflammation and thrombosis of the lymphatics is also very frequently met with in the uterus and in the surrounding pelvic cellular tissue. Generally it is the puerperal injury to the inner surface of the uterus, more rarely other diseases of this organ, which, apparently from infection ab externo, forms the starting- point of the tymphangifis. In these cases the lymphatics are found to be dilated and filled with an opaque, thick, purulent, or ichorous matter. The wall of the vessel, according to Duplay, A'irchow, and others, is at first normal, but may subsequently inflame and suppurate, which the surrounding connective tissue may also do. The lymphatics are specially apt to be disease* 520 QUINCKE.—DISEASES OF THE LYMPHATICS. in the posterior and lateral parts of the uterus, as well as in the broad ligaments of the uterus ; those of the false pelvis, the inguinal and femoral regions, are more rarely affected. Peri-uterine lymphangitis cannot be regarded as an idiopathic disease, since it is only a somewhat inconstant concomitant of the most diverse forms of puerperal disease, such as inflamma- tory parametritis, septic processes, and thrombosis of the uterine veins. The pathological and prognostic significance of this, as well as of other diseases of the lymphatics, does not so much depend upon its existence merely as upon the nature of the pro- cess in which it originates, and this also determines the nature of the treatment to be adopted. We know but little about inflammations of the thoracic duct, or of its morbid affections generally—partly, indeed, because but little attention is paid to it at post-mortem examinations. An- dral examined the thoracic duct with great care in three hun- dred bodies, and found it only five times pathologically altered. In one case thrombosis of its upper part was found, propa- gated by continuity from thromboses of the subclavian and jugu- lar veins ; the wall of the vessel was somewhat thickened, the lower part of the duct dilated (Oppolzer). In other cases the wall of the vessel was inflamed, its contents purulent, or thick, cheesj7-, tuberculous (Andral, Yelpeau, Worms, Gendrin, Cooper); the valves are in such cases thickened or adherent, the lumen often dilated. Calcification of the wall of the duct (Wrisberg, Mascagni) or of the contained thrombus (Browne Cheston) has been also observed. Finally, closure of the duct by adhesion throughout its entire length has also been seen as the result of inflammation. But little is known of the phenomena presented during life in inflammation of the thoracic duct. A priori, one would expect at one time narrowing or occlusion of the duct {vide infra)), at another the possible extension of the thrombosis into the subcla- vian vein, etc. In the case related by Worms, which seems to have been a primary inflammation of the thoracic duct, the dis- ease ran its course in fourteen days ; it commenced with violent pains in the body and fever, followed by swelling of the left arm, DEGENERATIONS AND NEOPLASMS. 521 thrombosis of the subclavian vein, pyaemic fever, icterus, and death. Degenerations and Neoplasms affecting the Lymphatics. Andral, Arch. gen. 1824. Tom. VI. p. 507.—Armauer-Hansen, Beitr. z. Anat. d. Lymphdr. 1811—Aufrecht, Med. Centralbl. 1869. No. 28.—Bastian, Edinb. Med. Jour. 1867. p. 815.—Cruveilhier, Anat. Pathol. H. Livr. 27. PI. 2.—Klebs, Virch. Arch. Bd. XLIV. S. 256.—Kbster, Virch. Arch. 1867. Bd. XL. S. 468. Die Entwickelung der Carcinome. 1869.—Th. Langhans, Die Lymphgefasse d. Brustdriise und ihre Beziehungen zum Krebse. Arch. f. Gynak. Bd. VIII. S. 1. 1875.—Pagenstecher, Virch. Arch. Bd. XLV. 1869. etc.—Recklinghausen, Arch. f. Ophthalm. 1864.—Rindjleisch, Patholog. Gewebelehre. S. 99.—E. Wagner, Krebs d. Lymphgefasse d. Pleura, u. d. Lungen. Arch. d. Heilk. IV. S. 538. It has already been stated that thickening of the coats of the lymphatics and hyperplasia of the connective tissue have been observed as the results of inflammation. Calcification of the walls of the thoracic duct has been also seen. No special refer- ence is to be found to any other form of degeneration. The lymphatics are frequently found to be implicated in cer- tain pathological neoplasms, such as cancer and tubercle. In both of these instances it happens in this way : cells, tissue juice, or cheesily-degenerated particles of the neoplasm are taken up directly by the smaller lymphatics, carried on some distance with the lymph-stream till they adhere to the walls of the vessel or are arrested within a gland, and here, partly directly from the tissue elements which have been floated off, and partly, second- arily, from the infected wall of the vessel, there occurs a further and fresh development of cancer or tubercle. Where glands interrupt the course of the lymph, the germs of the neoplasm seem not to be propagated in a centripetal direction until the gland itself has become diseased. Thus in tuberculosis of the epididymis, or of the intestines, the lymphatics of the spermatic cord and of the mesenteiy are by no means unfrequently filled with cheesy matter; Andral saw the lymphatics on the surface of tubercular lungs filled with similar contents ; and even the thoracic duct has been found filled with chees}^ material in similar conditions, in tuberculosis of the mesenteric and lumbar glands (Cooper). 522 QUINCKE.—DISEASES OF THE LYMPHATICS. In cases of tubercular ulceration of the intestines, Klebs saw yellow and gray tubercles within the lumen of the lymphatics, and could trace a series of tliese tubercles up to the nearest gland. On the other hand, Armauer-Hansen declares that these tubercles are always external to the lymphatics of the serous covering of the intestine and of the mesentery. Similar and often more striking observations are often made on the lymphatics of the peritoneum, of the diaphragm, and of the pleura, in cases of carcinoma of the intestinal tract, of the liver, and of the uterus. In such cases the lymphatics appear as extremely beautiful nodular cords and networks, which are completely filled with cancerous material. Rokitansky found the receptaculum chyli filled with cancerous matter in a case of carcinoma of the retroperitoneal glands ; Cruveilhier and Andral found the thoracic duct filled in the one case with cancerous matter, and in the other with cancerous matter and pus, in cases of uterine sarcoma. Cancer occasionally but much more rarely develops itself primarily from the walls of the lymphatics. E. Wagner ob- served an instance of this in the lymphatics of the pleura and lungs. According to recent authors, neoplasms frequently originate in the lymphatics. Klebs, Aufrecht, Rindfleisch, Bastian and others adopt this view in regard to tubercle, while Recklinghausen and others, particularly Koster, look upon carcinoma (of the skin and of the stomach) as originating in this way. We cannot now enter more fully into these observations, which only relate to the most minute lymphatics, and possess mainly an anatomical interest. But we must point out that Langhans is opposed to this view, and has not only shown the incongruence between the form of the normal lymphatic network and the network of cancer cells in the localities specified, but has also, on careful examination of the carcinoma mammae, been unable to recognize the lymphatics as the point of origin of the disease. During life it is impossible to recognize either tubercular or carcinomatous disease of the lymphatics. It may however be suspected whenever, in the course of any such organic disease, the lymphatic glands become swollen or the serous cavities diseased. The therapeutics of such an affection must be confined to prophylaxis. NARROWING, OCCLUSION, AND DILATATION. 523 Narrowing, Occlusion, and Dilatation of the Lymphatics. Alter, Generalsanitatsber. f. Schlesien. v. J. 1834. Breslau. 1836.—Anger, Des tumours erectiles lymphatiques. Paris. 1867.—Demarquay, L'Union medicale. lH'A.—Dexjardins, Gaz. mgd. 1854. Nos. 24, 27, 30, M.—Hugier, Bull, de la Soc. de Chir. T. II.—Labbe, Dilatation variqueuse des lymphatiques. Gaz.' des Hop. 1867. p. 421.—Laennec, Traite de Tauscult. med. 3d edit. III. p. 439. —Casuistische Angaben bei Lebert, S. 608.—Levin, Lymphangiectasis submucosa pereurrens. Nord. Med. Ark. VII. 2. 1874.—Magendie, Handb. d. Physiol. fibers, v. Heusinger. II. S. 160. Eisenach. 1836.—Morton, Phthisiologioe. Lib. I. Cap. 10. p. 21. in van Swieten, Comment IV. p. 189.— Oppolzer, Allg. Wiener med. Zeitg. 1861. No. 19.—R. Paterson, Congenital lymphatic varix. Edinb. Med. Journ. May, 1871.— Petters, Prager Vierteljahrschr. 1861. Bd. 4. S. 146. —Rokitansky, Pathol. Anatomie. Bd. II.—T. Grainger Stewart, On dilatation of the lacteals. Edinb. Med. Journ. 1863. p. 448.—Trelat, Gaz. des Hopitaux. 1869. No. 136.— Virchow, Arch. Bd. VII. S. 130. Ueber Makroglossie.— Wernher, Beitr. z. Kenntniss d. Elephantiasis Arabum. Deutsche Zeitschr. f. Chirurgie. Bd. V. S. 394. 1875. (Contains many references and extracts from relative literature.)—Wutzer, Midler's Arch. 1834. S. 311.1 Etiology. Very little is known in Tegard to abnormal uniform narrow- ness or dilatation of the lymphatics, either congenital or arising during development, and extending over a greater or less area. Alter observed a congenital ektasia of the jugular plexus: Paterson, one of congenital ektasia and varicosity of the superficial lymphatics of one leg. In the latter case there was swelling of the leg, condensation of the connective tissue over and around Poupart's ligament, and lymphorrhagia. Probably there was in this case a want of anastomotic connection between the superficial and deep lym- phatics. The individual variations in the calibre of the lymphatics must he even greater than those of the blood-vessels, because of the little constancy there is in regard to even their coarser topo- graphical relations ; but the collateral equalization of the lymph circulation is certainly more easily brought about. It is probable that the persistence of such abnormalities in the vas- cular lumen of the lymphatics is not without influence upon 1 Vide Lymphorrhagia. Infra, p. 532. 524 QUINCKE.—DISEASES OF THE LYMPHATICS. the nutrition of the area from which they spring. Narrowing of the ^ductus thoracicus and of the lacteals may prevent the sufficient absorption of nutritive material, and may thus (besides disposing to disease of the intestines) give rise to permanently defective nutrition and a stunted development. Of all pathological processes it is chiefly inflammation and thrombosis which give rise to circumscribed or more extensive narrowing, and frequently to complete occlusion of the lym- phatics : by thickening of their coats, adhesion of their internal surfaces, transformation of the vessel to a cord of connective tissue, or calcification of the coats of the vessel or of the thrombus. The lymphatics may also become narrowed or occluded by particles of tubercular or cancerous material, which, when floated off from their original site, may either themselves undergo further devel- opment or may occasion a similar morbid affection of the coats of the vessels. External compression from the cicatrization following inflammation of the connective tissue, or from tumors (such as aneurisms, cancerous masses, or glandular swellings, which may compress the thoracic duct), act also in a similar manner. If the compression be permanent and complete, inflammatory adhesion of the internal surfaces of the vessel results, the centripetal por- tion of the vessel becomes narrower up to the nearest collateral branch, the glands connected with the occluded vessel become small, hard, and dense ; within the entire area from which the narrowed or occluded vessel originates, there is lymph stasis, dilatation of the lymphatic trunk, and oedema of the tissues. Dilatation of the lymphatics also occurs, not only as the result of narrowing of the central trunks, but also within the area of diseased glands, through which the passage of the lymph is thus hindered. Under this head we may mention neo- plasms, chronic inflammation with hyperplasia of the connective tissue framework, or resulting in caseation. Stasis of the blood in the large veins, the result of cardiac disease (Petters, Op- polzer), must also be considered in connection with the thoracic duct, inasmuch as lymph stasis may thus be produced. In peri- pheral parts of the body, dilatation of the lymphatics is not unfrequently the result of repeated attacks of inflammations (erysipelas, inflammations of the connective tissue); excessive NARROWING, OCCLUSION, AND DILATATION. 525 exercise of function from repeated excessive flow of lymph, perhaps also slight inflammatory attacks of thrombosis of the vessels, seem to be the active agents in this case. In a number of recorded cases of dilatation of the lymphat- ics, no efficient cause has been discovered ; it is possible that some mechanical obstruction to the lymph stream was present and was overlooked. Yet we must not quite disregard the pos- sibility of an idiopathic dilatation, which may be produced by pathological alterations in the walls of the lymphatics them- selves, just as happens in the blood-vessels. Even a paralysis of the lymphatics, such as has been hypothetically assumed by Eramert and others, seems to be not a very improbable cause of dilatation, since unstriped muscular fibres have been observed in the walls of the lymphatics, and rhythmical contractions of tliese vessels have been observed in certain parts to assist the onward movement of the lymph-stream. Apart from the lymphatic hearts of the frog, which have been long known, Heller has observed contractions in the lymphatics of the mesentery of the guinea-pig, which, commencing close to the valves, forced the contents onwards, and had a rhythm of their own quite independent from that of every other movement. Anatomy. The dilated lymphatics are seen as cjdindrical, usually tortuous cords, which present nodular swellings in the position of the numerous valves, and often form a network. Their diam- eter may be double that of the normal vessels, and their varices may be as large as an apple. According to Rokitansky, their coats are sometimes thickened, and at others attenuated ; conse- quently rupture not unfrequently takes place, lymph is effused into the connective tissue or exernally, effused chyle forms easily recognizable white extravasations in the intestinal mucous mem- brane between the layers of the mesenteiy or in the peritoneal cavity. Within the area of dilatation the glands are somewhat en- larged, their lymph ducts distended, often so much so as to produce large, locular, cystiform tumors (Lymphadenectasiae). The contents of the dilated vessels is sometimes a clear, 526 QUINCKE.—DISEASES OF THE LYMPHATICS. watery, feebly opalescent, or turbid milky fluid; the turbidity, as in normal chyle, is caused by minute fatty granules ; more- over, this milky fluid is not only found within the area of the intestinal lacteals, but also in other parts (as the scrotum, thigh, etc.)—probably by means of dilated collateral anastomotic branches which reach these parts. Sometimes small quantities of blood are mingled with the fluid. When the stagnation has lasted some time, the lymph may become thickish or unctuous. Further, the dilated vessel may be partially or wholly filled with coagulated lymph, either recent or in various stages of metamor- phosis, or it may be filled with pus, cancerous or tubercular material. Symptoms. Both narrowing and dilatation of the lymphatics very often present no sj^mptoms during the life of the patient, either from the occult position in which they are situated, or because the disturbances produced by them are compensated by the dilata- tion of collateral vessels. Where narrowing or occlusion of a lymphatic trunk is brought to light, this happens through this dilatation of the collateral vessels or from the congestion of the area whence the radicles of the narrowed vessel spring. This congestion sometimes causes dilatation chiefly of the nearest- lying larger vessels {vide infra), at others the radicles themselves are affected, and within their area we have oedema and hyper- trophy (sclerosis) of the connective tissue produced, just as has been already noted when speaking of the results of lymphangitis. Under these circumstances the venous current seems, at least to some extent, to replace vicariously the interrupted lymph current. According to Emminghaus, so long as the venous current remains unimpeded, the formation of lymph is very trifling — at least within the cutis and subcutaneous layers of fat. Of all dilated lymphatics, those best known, and most easily observed, are those which run their course superficially. The most frequent seat of this alteration is the lower half of the body, particularly the thigh, the inguinal region, as well as the scrotum and penis, and its usual cause seems to be disease of the inguinal glands. NARROWING, OCCLUSION, AND DILATATION. 527 Quite a remarkable number of such patients have lived, at least for a time, within the tropics; in the case of many of them the glandular swelling was of syphilitic origin; one patient labored under caries of the bones of the foot; another had suffered from typhus two years previously; a woman, whose case is narrated by Buchanan, suffered for years from repeated attacks of fever, combined with inflam- mation of the leg (phlebitis or lymphangitis ?). In such cases we see lying, just beneath the unaltered or slightly discolored skin, cylindrical or varicose cords from one to several millimetres in diameter; tliese are usually specially distinct upon the penis, where they form a coronet surrounding the corona glandis and one or two cords extending upwards along the back of the penis. Moreover, particularly on the thigh and lower part of the abdomen, we find a considerable number of vesicles the size of sago-grains, often arranged in rows, which originate in the enlarged cuticular papillae, whose circum- ference is sometimes slightly swollen ; when tliese vesicles are pricked, or should they burst spontaneously, which often hap- pens, an opalescent, sometimes opaque, milky fluid escapes from them. A similar fluid is also sometimes discharged from scarcely visible capillary openings in the cutis. These originate in dilata- tion and rupture of the superficial lymphatic network of the cutis. A copious lymphorrhagia sets in when the larger dilatations are punctured intentionally or from an erroneous diagnosis. Xodu- lar varicosities of the lymphatics, the size of a filbert or apple, or masses of tortuous cords are also seen, particularly in the ingui- nal region. These are sometimes tense and full, at others softer, usually painless and capable of being diminished by pressure ; the lymphatic glands in this situation seem to assist in their formation. They may be confounded with femoral hernias, abscesses, or other morbid affections of the lymphatic glands. Such patients have no subjective morbid phenomena ; at the most they have a feeling of tension or slight stinging pain in the region of the swelling, which is diminished on the occurrence of a rupture. Slight weakness of the corresponding extremity is also felt, especially when the lymphorrhagia is profuse. In one case of cavernous lymphangioma of the thigh, which was incised, Gjorgevic observed a fibrinous layer on the coats of the vessels, also redness and infiltrations of the neighborhood, as often as the flow of lymph became obstructed. 528 QUINCKE.—DISEASES OF THE LYMPHATICS. Similar dilatations have been observed on the abdominal walls (Fetzer), on the anterior surface of the chest (Coley), and on the neck (congenital, Alter). In all cases they were slowly developed ; a declension of the phenomena or a cure was never observed. Dilatation of the lymphatics is not dangerous to life ; but should they become injured or ulcerated, inflammation and septic infection of the organism may very readily occur. The diagnosis is all the more easily made, the more super- ficial the vessels are. They are chiefly to be distinguished from dilated veins by their form, position, and color ; varices in the inguinal region are distinguishable from herniae by their con- sistence and by their never containing air ; corded lymphatics are also usually to be detected in the neighborhood of these varices. Varices may also be mistaken for tumefied lymphatic glands, but they are softer than simply swollen glands ; they are also to be distinguished from abscesses by their slow develop- ment and painless character. The diagnosis is much simplified by the formation of vesicles and the occurrence of lymphorrhagia. The treatment must be partly directed to the prevention of any increase of the dilatation, by uniform pressure, by means of appropriate bandages (elastic—or lacing—stockings, suspensory bandages, etc.), and partly to the production of thrombosis or occlusion of the dilated vessels. With the latter intent, caustics may be employed, or threads soaked in alcohol may be drawn through the vessel. This procedure can only be considered rational when we have only to do with a simple dilatation and when there are sufficient collateral means of removing the lymph. When however the dilatation is the result of a central obstruc- tion to the lymph stream, such measures can only increase the lymphatic congestion, or, at the most, cause the dilatation to be transferred to some other trunk. Circumscribed dilatations and cavernous lymphatic tumors have been successfully extirpated. Wernher regards a dilatation of the lymphatic capillaries of the corium as the actual cause of elephantiasis (Arabum). Extravasations of lymph and dilatations of the larger lymphatics are also present. Teichmann could trace, by means of injections, this lymphatic dilatation into the hypertrophied cuticular papillae. NARROWING, OCCLUSION, AND DILATATION. 529 Gaetani was able to express sixty per cent, by weight of lymph from a piece of excised skin.—W. distinguishes this true lymphatic elephantiasis from those pachydermatous and connective-tissue hyperplasias which are prone to accompany varicosity of the veins, and which resemble it in external appearance. The cause of this dilatation, according to W., can only very rarely be proved to depend upon lymphatic congestion, the result of inflammation of the glands, and the obliteration of the larger trunks. Gravity, as in dilatation of the veins, seems to exert an im- portant adjuvant influence. Next to the lower extremities, the scrotum and mammae are most frequently affected ; hydrocele is not an unfrequent concomitant. The inflammations which attack parts affected with elephantiasis, according to W., are to be regarded as results rather than causes of the lymphatic conges- tion. For treatment, compression and ligature of the main artery of the limb have been recommended. Instead of these, W. recommends the less serious measure of methodic compression; but neither of these treatments is said to have any per- manent result. Partial excisions and incisions of the skin would seem to be more useful, as by their cicatrization the lymphatics are partly occluded. Levin observed several times in himself a colossal swelling of the right half of his upper lip, which developed spontaneously in fifteen minutes, and disappeared in half an hour. He fancied this to be a temporary dilatation of the submucous lym- phatics (possibly a rupture (?)—Q). Virchow and Textor saw an enlarged tongue (makroglossia) in a girl two years of age, produced by dilatation of the lingual lymphatics ; these had given rise to a series of cavernous spaces. The existence of narrowing or dilatation of the deeper lying lymphatics can be only suspected, when there is at the same time dilatation of the superficial lymphatics, when the lymphatic glands over a considerable area or when main lymphatic trunks are diseased, or when oedema occurs, which is not explicable by any obstruction to the venous blood-stream. NARROW! N< J- AND DILATATION OF THE DUCTUS THORACTCUS. Narrowinu; or occlusion of the ductus thoracicus is brought about by i.iiianimation of its coats, by blocking of its lumen with masses of a simply cancerous or tubercular thrombus, by the compression of cicatrices, aneurisms (Laennec, Bennet), can- cerous tumors (Virchow), or tubercular glands within the medi- astinum (Otto, Morton). The narrowing sometimes affects only a limited portion of the duct; at others this is obliterated through- out its whole extent. VOL. VI.—34 530 QUINCKE.—DISEASES OF THE LYMPHATICS. The duct is often dilated above the narrowed portion; but this is by no means constant, and is all the more likely to be absent the more gradually the obstruction has occurred. In such circumstances a collateral circulation is carried on by one of those re-entering duplications of the thoracic duct (such as Astley Cooper observed in a case of its occlusion), or by one of the hepatic or thoracic lymphatics. Even ligature of the thoracic duct, which was repeatedly carried out in horses by Dupuytren, is not always, as Magendie reports, followed by the death of the animal from obstruction to the onward flow of the chyle, but is often compensated by the establishment of a collateral flow. Rohrig also observed the flow of chyle to pass collaterally through the neck and thoracic walls in dogs who had their thoracic ducts ligatured. Varieties also occur in regard to the situation in which the lymphatics enter the veins, as Tiedemann and Fohmann tell us. Wutzer saw the thoracic duct terminate by two parallel branches in the vena azygos on the hither side of the occluded part. Dilatation of the thoracic duct is also brought about, apart from the causes specified, in certain cases of cardiac disease, by the resulting venous congestion (Rokitansky, Petters), as well as by unknown causes. Rokitansky found it once in the body of a lunatic who had been tormented with insatiable hunger. Andral found the thoracic duct occasionally dilated on the thither or central side of a contracted part, just where the collateral vessels entered. This dilatation usually extends as far as the receptaculum chyli and the mesenteric lymphatics ; sometimes also the latter alone are dilated, and only in certain parts of the mesentery; the smaller vessels of the intestines and of the peritoneum may then be dilated in the form of cords and vesicles, and extravasa- tions of chyle may occur within the mesentery and in the walls of the intestines ; chylous fluid in considerable quantity has also been observed free within the peritoneal cavity. The chyle within the dilated vessels is usually inspissated or coagulated. Rokitansky has described a typical case, a woman aged sixty-two, with sub- cutaneous oedema and very considerable milky effusion into the sacs of both pleurae and of the peritoneum, with dilatation and hypertrophy of the heart, thickening and shortening of the mitral valve, thickening of the pyloric half of the coats of the stomach, the intestinal villi turgid with a whitish fluid. The subpleural NARROWING, OCCLUSION, AND DILATATION. 531 lymphatics of the lungs were distended, the lacteals and the thoracic duct in the following condition: "They were for the most part, especially from the intestine to the nearest range of glands, mostly nodularly dilated, and stuffed full of a whitish, soapy, unctuous mass, which broke down uniformly in water, to which it communi- cated a slight opalescent cloudiness. This mass consisted of an agglomeration of fatty granules, crystals of margarine, oil globules, and a few cells, some of which contained nuclei of considerable size. In isolated spots, particularly at the varicose nodosities, the mass was of a more yellowish color, and adhered to the walls of the vessels. At tliese parts the vessel was covered with a network, and was here and there quite occluded. The meshes of this network contained agglomera- tions of fatty granules. The glands were not much enlarged, and were here and there speckled with white." The receptaculum chyli and vessels entering it were dilated, their coats thickened; the former was lined internally with a grayish-red reticulated stratum, from which a nodular excrescence here and there protruded, or a filamentous bridge extended. The thoracic duct was occluded by a similar soapy material, partly filled with indurated material, and quite blocked up. In one case observed by Dr. Fetscherin and myself, the occlusion of the lacteals, when they passed from the intestine into the mesentery, was caused by inflammatory thickening of the latter (Langhans); yet in this case the congestion of the lacteals and the extravasation of the chyle into the coats of the intestine and into the peritoneal cavity were very complete. The right pleural cavity was filled with a milky fluid; elephantiasis of one leg was also present. The latter ailment had occurred several times previously in the family of this young woman, who was thirty years of age. Symptoms. Narrowing and occlusion of the ductus thoracicus, like dilata- tion, often give rise to no symptoms whatever during life, espe- cially in those cases of slow occurrence, in which, as already narrated, both lymph and chyle readily find collateral routes. In other cases, the results of the lymphatic congestion come to light even during life, especially within the area of the lacteals. Ascitic fluid, often to an enormous amount, is effused, and, in spite of efficient removal by paracentesis, it is rapidly renewed. The fluid drawn off is sometimes clear like lymph (Petters), at others turbid from suspended fatty molecules (Oppolzer), or milky (Morton, Marshall Hughes). Both appetite and nu- trition were defective as the result of the obstructed absorp- tion ; the urine was scanty, partly from the same reason, partly from the presence of the ascites. In one case, related by Roki- 532 QUINCKE.—DISEASES OF THE LYMPHATICS. tansky, not only the peritoneal, but also the pleural cavities were filled with chylous effusion. Death resulted partly from the original disease (valvular cardiac disease and venous conges- tion), and partly from the mechanical results of the effusions mentioned. CEdema of the lower extremities does not seem to be a neces- sary result of occlusion of the thoracic duct, at least no mention of it is made in the solitary uncomplicated case related by Mor- ton. For tliese parts, therefore, other lymph routes, or even the veins, seem to act vicariously. The treatment can only be palliative ; where there is general venous congestion, the cardiac force must be regulated. Any considerable amount of ascites necessitates tapping, which must indeed be generally repeated in a very short time, on account of rapid reaccumulation. Rupture of the Lymphatics. Lymphorrhagia. Bergcret,~De l'ascite huileuse. Jour, d'anat. et de phys. de Robin. Nov. 1873; Lyon medical. 1874. p. 305.—Bonet, Sepulcretum. IV. Sect. VII. Obser. XXIV. p. 360.—Bourdon, Journal de Savants. 5 Juin, 1874; Schmidt's Jahrb. 123. S. 274.—Buchanan, Escape of chylous fluid from the thigh. Med. Chir. Transac- tions. XLVI. p. 57. 18G3.—Canton, Edinb. Med. Jour. Jan. 1860. p. 690.— Carter, The British Med. Jour. 1862. March 25; Med. Chir. Trans. XLV. p. 189. 1862.— W. H. Day, Lymphorrhcea. Med. Times and Gaz. April, 1869.—Demar- quay, Memoire sur un cas de lymphorrhagia. Mem de la Soc. de Chir. de Paris. T. III. p. 139.—Desjardins, Gaz. med. de Paris. 1854. No. 24. Lymphatic fistula. —Durand Fardel, Traite des maladies des vieillards. 1854.—Emminghaus, Physiologisches und Pathologisches iiber die Absonderung und Bewegung der Lymphe. Arch. d. Heilk. 1874. S. 308 u. S. 329. Notices of the literature on the subject.—Friedel, Beitr. zur Kenntniss des Klimas und der Krankheiten in Ostasien. Berlin. 1863. S. 123.—Gjorgevic, Ueber Lymphorroe und Lymphan- gioma Langenbeck's Arch. Bd. XII. S. 641. 1870. Literature of the subject.— Golgi, Virch. Arch. Bd. 51. S. 568.—Sigismund Grass, Ephemerides Germanise decur. I. ann. IX. u. X. Vratislav. et Bregae. 1680.—Guiffart, Bei Bartholin. Oper. Nov. p. 490.—Hensen, Ueber die Zusammensetzung einer als Chylus auf- zufassenden Entleerung aus der Lymphfistel eines Knaben. Pfliiger's Archiv. X. 1875. S. 95.—Hilton, Lancet. 1866. II. p. 37.—Hoffmann. Opera Suppl. II. Pars II. 1704. p. 460.—Hoppe-Seyler, Pfliiger's Arch. VII. 1873, S. 407.— Marshall- Hughes, A remarkable case of abdominal effusion (chylous) resulting from RUPTURE, LYMPHORRHAGIA. 533 mesenteric tumor. Guy's Hosp. Rep. 1841. p. 297.—Munson, The Medical Record. 1 May, 1873.—Maur<>, Donald, An essay on the dropsy and its different species. London. 1756.—Odenius, Fall von Lymphorroe, Pachydermia lymphor- rhagica. Nord. Medic. Ark. VII. 2. 1874:.—Petters, Ueber Lymphorrhagia.— Klebs, Ueber Lymphangiectasie. Prager Vierteljahrschr. 125. Bd.— Quincke, Deutsch. Arch. f. klin. Medic. 1875. Bd. 16. S. 121.—Rommel, Ephemerid. Ger- maniae decur. II. ann. VIII.— Rudolphi, Ueber die Todlichkeit derWunden des Brustganges. Casper's "Wochenschr. f. d. Heilk. 1835. Nos. 41-43.—Battler, Lymphextravasate. Zeitschr. f. "Wundiirtze und Geburtshelfer. Heft 2 u. 3.1871. — Scholz, Wiener med. Wochenschr. 1868. No. 63.— Wienkowski, Lymph- gefiissfistel. Wiener, med. "Wochensch. 1871. No. 33. Laceration of the smaller lymphatics, as well as of the blood- vessels, is sure to occur in every variety of injury, surgical operation, contusion, etc., although it may not be recognized, on account of the transparency of the lymph; very probably effusion of lymph contributes not a little to the swelling of the tissues following an injury, and the secretions of wounds them- selves may also be largely composed of lymph. From the thinness of the walls of the small lymphatics, we may also readily assume that their rupture may, at least occa- sionally, be brought about by occlusion of the larger trunks by lymphangitis. The results of this are of no importance, as the tyniph effused into the tissue spaces is speedily taken up by other lymphatics. Even the oedema which occurs, especially in the lower ex- tremities, in hydrsemia and general venous congestion, may also he accompanied by rupture of the smaller lymphatics. Possibly it is nothing else than this that occurs when the overstretched skin spontaneously bursts and serous fluid escapes externally. It is, however, no doubt true that the oedematous fluid which thus spontaneously escapes, or is obtained by puncturing the subcutaneous cellular tissue, is much more watery than the lymph obtained from larger lymphatic fistulse {vide infra). O. Weber, for example, found onty 1.9^ of solid contents in it. The larger lymphatics rupture either as the result of wounds, previous disease, or, more frequently, after they have been from an}- cause dilated and their coats thinned. Only six cases of rupture of the thoracic duct have been recorded. It was caused by perforation of the left side of the chest with a knife, the 534 QUINCKE.—DISEASES OF THE LYMPHATICS. opening of an abscess (Hoffmann), gunshot wound of the spine (Bonet), or the being run over by a carriage (Quincke). The symptoms of lesion of the thoracic duct were somewhat obscured by the other results of the injur}^. In three of the cases a white chylous fluid escaped from the wound externally. In the case related by Hoffmann, this fluid was observed to be thicker or thin- ner, according as the patient had ingested solid or fluid nutriment. In Bonet's case the escape of the yellowish white fluid commenced fourteen days subsequent to the receipt of the gunshot wound, and lasted, with the exception of an intermission of two weeks, till the death of the patient, which was partly occasioned by fever and exhaustion, and partly apparently as the result of injury to the spinal cord (epi- leptic attacks and hemiplegia). In the cases related by Monro and the author, the chyle was effused into the pleural cavity. In the second of these cases, the right pleural cavity was so dis- tended by the effusion that it had to be repeatedly tapped. Nevertheless, the effusion was so rapidly renewed that the patient died on the twenty-first day from interference with the respiratory and cardiac movements. There never was any fever or pain in the side. At the dissection seven litres of chylous fluid were found in the pleural cavity, which was otherwise perfectly healthy. The fatal termination had been indubitably hastened by the withdrawal of such a large quantity of nutri- tive fluid from the circulation, part of it also having escaped externally. In the case observed by Guiffart, lymph and chyle were effused into the mediastinum, and caused death by suffocation. According to these cases, the diagnosis of injury to the thoracic duct is most uncertain. It attains probability when pleuritic effusion is developed without inflammatory phenomena or fever subsequent to an appropriate etiological cause, but it only becomes certain when chylous fluid escapes from a wound or is withdrawn by tapping. The prognosis is usually fatal, yet, according to the second case mentioned above, the continuance of life seems to be pos- sible, and even a cure does not seem to be absolutely impossible, since, from the trifling intravascular pressure, a small wound of the wall may very readily close up. The treatment can only be symptomatic. Rupture of the lacteals within the abdominal cavity and effusion of chyle into it has been observed a few times (Mun- son, Hoppe-Seyler) ; in one of these cases the cause was obscure, and the discovery of the rupture was only made accidentally at RUPTURE, LYMPHORRHAGIA. 535 the dissection; in the other there was congestion of the lym- phatics from the pressure of a tumor. Precisely similar results, as those arising from the rupture of one of the large lymphatic trunks, may be produced by the rupture of many lymphatic capillaries, which may be caused by congestion of the lacteals by closure of the thoracic duct (Morton, Rokitansky) of one of the larger lacteals (Marshall Hughes), or of several of the smaller lacteals within the mesentery (Langhans ; the author). In all tliese cases there was effusion into the peritoneal cavity, which from its amount produced considerable disturbance, and which after repeated tappings always reaccumulated with considerable rapidity. The fatal result was partly due to the original disease and partly to exhaustion and the evil results produced mechanically by the ascitic effusion ; in several cases the affection lasted from five to six months, and as many as ten tappings were made. Where there is no congestion, or where the ruptured vessel is small, it may heal without producing any marked symptoms; Monro even saw a wound of the receptaculum chyli, in a pig, close very rapidly by the formation of a clot. For the peritoneum as well as for the pleura the chyle is a perfectly indifferent fluid, which never produces the slightest inflammatory irritation. A part of the effused chyle is, more- over, taken up and removed not only b}^ the blood-vessels, but also by the lymphatics of the peritoneum ; at least this seems to have occurred in one case in which (the thoracic duct being per- fectly pervious) traces of chyle were also found in the pleural cavity. All tliese cases are of considerable physiological interest, inasmuch as they afforded an opportunity of examining human chyle, pure or mixed with some serous transudation. The specific gravity varied from 1007 to 1016, the fatty contents from 0.5 to 1.8 per cent. The fluid also contained a quantity of albumen, traces of peptones (but no traces of any albumen decomposing ferment, Hoppe-Seyler), small quantities of fibrine, cholesterine, diastatic ferment, and only a few lymph globules. On standing, a layer of cream is formed; it resists decomposition for a remarkably long time. Solutions of continuity in the large peripheral lymphatics, especially on the surface of the body, are very much more fre- 536 QUINCKE.—DISEASES OF THE LYMPHATICS. quently observed than ruptures of the lymphatics of the thorax or abdomen. Sometimes they are accidentally injured in perform- ing some trifling surgical operation (venesection, opening of a bubo or of an abscess); at other times dilated lymphatics are in- cised or punctured from a mistaken diagnosis; and at still other times the coats of the vessel are opened into by ulceration. Superficial thin-walled and dilated lymphatics may be also burst by muscular exertion or an unimportant blow. Rupture of the lymphatics is most frequently observed in the inguinal region, because dilatation of the lymphatics is most commonly observed in that region. According to the size of the ruptured vessel, the lymph escapes drop by drop or in a thin stream; in the latter way specially when pressure is made upon a turgid lymphatic. Movement of the limb affected considerably increases the flow of lymph, as in a physiological experiment. In the upright posture the flow of lymph has been frequently observed to be more copious than in the recumbent. But it may also undergo variations from other causes—may even dry up for weeks, and again recur, often very copiously. The effused fluid was some- times serous, yellowish, slightly opalescent, at others of a milky whiteness. Usually it coagulated spontaneously, though loose- ly ; a few times it was observed to redden on exposure to the air. On microscopic examination it was found to contain lymph globules and fat in fine molecular globules in various quanti- ties, sometimes red corpuscles. The reaction was alkaline, the specific gravity very various. In 100 parts of the fluid there were: Fetzer's Case. Desjardirts Case. Water.................... 93.68 93.99 Albumen................. 4.73 4.275 Fibrine...................... 0.56 Fat....................... 0.029 0.382 Salts..................... 0.95 1.3 Extractives............... 0.83 .... Ashes of the alcohol ex- tractives.................... 0.73 Traces of iron and sugar. RUPTURE, LYMPHORRHAGIA. 537 In Desjardin's case the lymphorrhagia was particularly copious, lasted forty-eight hours, and produced eleven pounds of lymph. In other cases only one pint escaped in a few hours. This depends upon the degree of vascular turgidity and the freedom of anastomosis with the injured vessel; when the out- flow is copious, the neighboring tissues or the swollen limb may evidently diminish in size. The copious fatty contents of the fluid in many of these cases permits the assumption that it contained chyle. And this was specially evident in the case narrated by Hensen of a ten-year- old Brazilian boy afflicted with a scrotal fistula. In it the fatty contents of the fluid could be shown to vary with the amount of fat ingested. The amount of Fat observed varied from 0.28 to 3.96 per cent. Albumen............ " 1.7 to 3.9 " Cholesterine......... " 0.018 to 0.102 " Salts.............•... " 0.643 to 1.09 " Water.............. "91. to 96.3 " Also, small quantities of sugar and fatty acids. It remains unexplained how in this case the chyle found its way into the peripheral lymphatics ; even on the supposition of considerable dilatation of the anastomosing branches, there must have been in part of them a lymph current in a direction contrary to the normal, which could only be made possible by insufficiency of the valves, and which was probably caused by gravity. After ligature of the thoracic duct in dogs, Rohrig' could frequently trace chylous congestion into the lymphatics of the kidneys and muscles, especially in aged animals. Lymphorrhoea onty influences the general health when it lasts for a very long time and is very profuse ; it debilitates like every other loss of the vital fluids; and the patient has a feeling of weakness, especially in the limb affected. Evil results from in- spissation of the blood, such as Lesser observed when experi- Ber. d. k. sachs. Ges. d. Wissenschaft. 1874. 538 QUINCKE.—DISEASES OF THE LYMPHATICS. menting upon animals, can hardly occur in men who can eat and drink. The prognosis in regard to life is therefore generally favor- able. Should the discharge come from a recent wound in a nor- mal vessel, a cure is generally possible ; but should it come from a vessel already dilated, a permanent fistula usually results, because from the persistent obstruction to the onward flow the lymph escapes under considerable pressure, and its constant flow hinders the closure of the opening. The treatment in recent cases must be confined to elevating the part affected, and keeping it as much as possible at rest, at the same time compressing the wound. When this is not suffi- cient, a variety of caustics have been applied to the wound. A similar procedure has been adopted in regard to the fistulae of dilated lymphatics. These measures have been adopted with the view of producing the complete occlusion of the affected vessel. Large losses of lymph necessitate the use of appropriate nu- tritives, ultimately of iron and bitter tonics. CHYLURIA. Golding-Bird, Lond. Med. Gaz. Oct. 1843.—Carter, On the connection between a local affection of the lymph-system and chylous urine. Med. Chir. Transac- tions. XLV. 1862, p. 289, contains notices of literature.—Eggel, Deutsch. Archiv fiir klin. Med. XI. S. 540. 1873. Literary notices here also. S. 427.— Pandurang Gopal, Med. Times and Gaz. 1873. June, p. 651.—Amyol,Ih\d. 1873, July.—F. H. Welch, Lancet. I. 1873.—Cunningham, Lancet. I. 1873.—T. R. Lewis, On a haemotozoon inhabiting human blood; its relation to chyluria and other diseases. Calcutta. 1872: quoted in Med. Times and Gaz. March 22d, 1873.—Do., The pathological significance of nematode haematozoa. Calcutta. 1874. Med. Times and Gaz. 1875. I. p. 173.—IF. Oehme, Fall von intermittir- ender Chylurie. Deutsch. Arch, fiir klin. Med. XIV. S. 262. 1874.—J. Crevaux, Journal de l'Anat. et de la Physiol. XL 2. p. 173. 1875.— Wm. Roberts, On renal diseases. London. 1872. Bibliography. In connection with lymphorrhagia I have now to speak of chyluria, inasmuch as it most probably is nothing else than an escape of chyle into the urinary passages. In this affection the urine has all the appearance of milk, and, like chyle, on standing it throws up a layer of cream. Very often a loose coagulum CHYLURIA.—ETIOLOGY. 539 separates on standing, and this is sometimes somewhat colored by red corpuscles. In one case, related by Carter, the white or pale red coagulum is said to have become distinctly reddened on exposure to the air. Microscopically we find an innumerable number of excessively minute (fat) globules as in chyle, sometimes red, more rarely white blood corpuscles, no renal cylinders. The reaction of the recent urine is acid. Besides the normal constituents of the urine, we find also the following substances (the figures are taken as a sample from the case described by Eggel). Albumen coagulable by heat........... 0.32—0.63$ 'Rt;"; ".........................1 0.2 —0.69. (Jholesterine.....................) Traces of lecithin; fibrine ; no sugar. When shaken with ether, the urine is freed of fat, and becomes quite clear. Quite recently Lewis has found in the urine the microscopic animalcule presently to be described, which he has named the " filaria sanguinis hominis." Etiology. This disease occurs endemically in certain tropical districts (Brazil, Mauritius, Isle of Bourbon, Bombay, and the West Indies) and also in South Carolina and Queensland, often side by side with the hematuria, which also prevails endemically in these districts ; moreover, the patients in tliese parts pay but little attention to it. In Europe also it has been (with the exception of a case related by Prout, one quoted by Golding Bird, another hy Cubitt, narrated by Beale, a fourth recorded by Roberts, and a fifth by^ Oehme) exclusively observed in those individuals who have passed at least a portion of their lives in the tropics. It is very remarkable that it has occasionally been first developed a long time (even so long as eighteen years) after leaving the trop- ics. It occurs cliieflv in middle life, rarely in children or in advanced life [of thirty cases collected by Roberts three were 540 QUINCKE.—DISEASES OF THE LYMPHATICS. under twenty, seven between twenty and thirt}T, eleven between thirty and forty, six between forty and fifty, and three over fif ty. The youngest case is mentioned by Prout—a male infant of eighteen months ;—the oldest by Quevenne and Crevaux, in which the patients were respectively seventy-eight and eighty.—Tr.]. Men and women seem to be nearly equally affected [of the thirty cases above referred to, nineteen were males and eleven females. When the disorder is endemic, it is said to be more common among women than among men.—Tr.]. According to Crevaux, the disease is most apt to occur during the hot season of the year. Symptoms. Apart from the condition of the urine, the morbid symptoms are generally trifling. A few patients complained of pain in the region of the kidneys, generally on both sides, more rarely on one side only, sometimes radiating towards the scrotum and upper part of the thigh. Dysuria is also sometimes produced by the spontaneous coagulation of the urine in the bladder. It is only at the commencement of the disease that the general health is somewhat disturbed (bodily weakness and mental de- pression, the urine then also usually contains more blood); subsequently the organism seems to get used to the loss of the vital fluids. The variations in the conditions of the urine are remarkable, as in the space of a few hours it may become clear and again milky. Bodily movement and the ingestion of food favor the occurrence of chylous urine; whilst, by fasting and continuance in the horizontal posture, it becomes clear. For this reason the urine passed during the day is usually milky, and that passed during night normal; in Outline's case this was reversed, and continued to remain so even when the patient kept his hid for forty-eight hours continuously. Quite independent of these daily variations, the disease also j varies within yet longer intervals of time, so that it may disappear for months or years, and again suddenly reappear. Crevaux quotes the case of a lady of the Isle de Bourbon, aged eighty, CHYLURIA.—NATURE OF THE DISEASE. 541 who for fifty years had suffered from chyluria and hematuria. Usually the disease at last ceases spontaneously. According to Lewis, deafness, diarrhoea, chronic conjunctivitis or more serious affection of the eyes, sometimes transitory swell- ings of the face and of the extremities, occur in connection with chyluria. Patients affected with chyluria often suffer simultane- ously from elephantiasis of the lower extremities and of the scrotum, or from dilatation of the lymphatics and lymphorrhagia in the inguinal region. In one case of Carter's, chyluria some- times alternated with lymphorrhagia or with swelling of the lymphatic glands. Niemeyer and Eggel found in one case fatty molecules (from five to ten times more numerous than the red blood globules) in blood removed by cupping-glasses ; a French observer (Guibourt) has made a similar observation, but not in every case. Lewis drew blood from the fingers by pricking with a needle, and found in it precisely the same little worms as in the urine. Nature of the Disease. Up to quite lately we were all in the dark as to the true cause of this disease, which is so rare with us, and in its course is so "capricious," as Rayer has termed it. The absence of any pertur- bation of the nutrition made any general disturbance of the inter- change of material very problematical, and the occasionally per- fectly normal character of the urine permitted the exclusion of an}T serious disease of the renal parenchyma. In both respects also the rare post-mortem examinations gave only negative results. The most probable explanation of the phenomena seemed to be the assumption of a lymphorrhagia into the urinary passages, because the condition of the urine would be thus efficiently ex- plained, and because other lymphorrhagias intermit in a similar manner, and are also similarly influenced by corporeal position, movement, and the ingestion of food. Anatomical proof of such a supposition was certainly wanting, and it was uncertain whether the admixture of chyle took place in the kidneys or lower down in the urinary passages. 542 QUINCKE.—DISEASES OF THE LYMPHATICS. A perfectly new light was thrown upon this disease by the discovery in such patients, by T. R. Lewis, of the embryo of a round worm, which he named the filaria sanguinis hominum. This is 0.35 mm. long, and 0.0075 broad, is contractile, finely striated transversely, and transparent, with a flat ribbon-like appendix at each end ; these animals are sexually immature. They exist in numbers in the blood of chyluric patients during life ; Lewis estimates the total number in the blood of one patient to be 140,000. The same animals are also very frequently found in the urine, inclosed within coagula ; they have been occasionally found in the (cholera) stools, and in the milky secretion in con- junctivitis. On dissection they were also found in the kidneys, in the supra-renal capsules, in the parenchymatous tissues, as well as in all the arteries and veins. The renal pyramids had a tallowy appearance, and along the urinary canals there were visible somewhat varicose tubuli with an oily lustre, which re- mained unaltered on the addition of warm ether, and seemed to be occluded lymph or blood vessels. According to Lewis, chyluria and many of its accompanying symptoms, probably also the endemic elephantiasis of the tropics, are caused by the presence of this parasite. Further inquiry must however determine the special manner in which this is brought about; it seems possible that the great numbers of these animals circulating in the blood occlude the blood-vessels and lymphatics, or that the encapsuled animals (as in dogs, etc.) form small tumors lying along the blood-vessels, and rupture of the capillaries occurs as the result of mechanical congestion. The development and migration of these animals has not yet been investigated. In the blood of the Paria dogs, according to Lewis and others, there are similar filaria embryos, which he and Welch at first supposed to be identical with those of man, whilst Cunningham, and subsequently Lewis himself, regarded them as of a different species. The mature specimens of this canine filaria are 25-90 mm. long (the females twice as long as the males), and they are found in tumors the size of a pea or walnut lying along the oesophagus and the thoracic aorta; they are also found within the coats of the aorta, in small tumors like tubercles, which now and then lead to bulging and ulceration of the intima; finally, they are also found in the lymphatic glands at the base of the heart. The females contained only ova, never free embryos. [Dr. Cobbold regards these nematoid haematozoa as identical with Bilharzia.—Vide Brit. Med. Journ. June, 1876, p. 780.—Tr.] CHYLURIA.—TREATMENT. 543 Though, according to these investigations, it seems almost certain that most cases of chyluria are caused by this hremato- zoon, yet it is always possible that in isolated cases, particularly in indigenous cases (such as that of Oehme, etc.), there may exist other causes of lymphorrhagia into the urinary passages, just as we also know that elephantiasis and lymphorrhoea may certainly occur quite independently of the presence of these parasites. Treatment. Before all things, it is needful to supply appropriate nourish- ment to replace the loss of the nutritive fluids. In opposition to this, Bouchardat, who supposes that there is an abnormal amount of fatty matter in the blood, recommends a diet poor in fat, car- bohydrates, and alcohol. Such a regimen is said to be commonly employed in the Isle de Bourbon. There also cold bathing is employed, and a change of climate recommended as soon as possible. In regard to medicaments, gallic acid has been employed with good results by Bence-Jones, in quantities of from one to two drachms per day. Besides this, other astringents, such as quinine and preparations of iron have also been used. Rayer gave tincture of cantharides in doses of from six to ten drops in the day. Harley recommends the internal use of iodide of potassium, and also its injection into the bladder, fifteen grains to three ounces of water, to kill the worms; oleoresin of male fern has also been used as an injection. Salesse employed copaiba. DISEASES OF THE PERICARDIUM. BAUER. DISEASES OF THE PERICARDIUM. History. Anatomical changes in the pericardium, especially pericar- dial exudations, were recognized long before ' the diseases of the heart itself were systematically described. Galen described peri- cardial effusions which he found in animals and suspected in men. Sal. Diversus, Forestus, and Rondelet saw and wrote about the pathological changes in pericarditis; Guarinoni and Jacutus Lusitanus observed them associated with pleuritis. The state- ments, however, concerning the frequency of these diseases and the idiopathic inflammatory nature of the effusions, were incom- plete, and the description of the disease associated with tliese changes does not altogether correspond with them. Thus Ron- delet described the disease with symptoms of fever, dyspnoea, pain under the sternum, and attacks of syncope. So, likewise, Riolan described it as follows: "Pericardium ipsum particeps esse potest inflammationis dolorificae et valde periculosse quia vicinum corcli, ac proinde patitur frequentes syncopas, tumque pulsus celerior, febris auctior, sitis vehementior quam in pleuritide aut inflamniatione pulmonum. Ssepe in eo copiosus humor col- ligitur qui suffocationem adfert et cor obruit. Si non possis exhaurire istud per hydragogen, licetne terebra sternum aperire intervallo pollicis a cartilagine xiphoide ?" a 1 The fables about the occurrence of hairy hearts in men distinguished for bravery and daring, robbers, etc., such as Leonidas, Lysander, Aristomenes, and others, are doubtless based on the discovery of stringy fibrin deposited on the heart.—Haller, Elem. Phys. Tom. I. ? Ench. Anatom. Lib. III. c, 4. / 548 BAUER.—DISEASES OF THE PERICARDIUM. In the eighteenth century, when the knowledge concerning heart diseases made such rapid strides, we find, in the works of the authors on that topic, numerous anatomical observations of dis- eases of the pericardium as well. Vieussens often met with ad- hesion of the heart to the pericardium at autopsies, and assigned certain functional disturbances during life to the existence of this condition ; whereas, in earlier times, it had repeatedly been considered to be a congenital defect. Albertini rightly appreciated the difficulties of a symptoma- tological recognition of pericardial effusions ; Morgagni arrived at the same conclusions, both by reviewing the work of others and by his own personal investigations, and believed, on account of the difficulty of diagnosis, that the day was yet remote when we should have recourse to the puncture of the pericardium recom- mended by Riolan. Senac also could not overcome the difficul- ties in diagnosis, which the obscure and inconstant symptoma- tology of these diseases made apparently insurmountable. In hydro-pericardium, Senac thought that he recognized an undulatory movement between the third and fifth ribs ; and al- though this sign proved to be erroneous, yet it was the com- mencement of the study of objective signs. Corvisart, who indeed did not see the above sign, but states that he felt it, first made the distinction between inflammatory exudations and dropsical effusions, which before his time had been generally confounded even by Senac and Morgagni, but he was unable to lay down any fixed rules for diagnosis. Auenbrugger first gave some accurate physical signs, such as bulging of the precordial region and also increase of percussion dulness. Nevertheless Laennec doubted the possibility of diagnosing pericarditis with certainty. These difficulties in diagnosis disappeared after the discovery of the pericardial friction sound by Collin (1824), and, thanks to the numerous works which followed close upon this, pericarditis at the present day can be classed among those dis- eases whose physical diagnosis is most complete and sure. They are mostly investigators in the field of heart diseases in general to whom we are indebted, and above all we should mention Louis, Bouillaud, Mayne, Latham, Haclie, Gendrin, Graves, Stokes, and Skoda. In most modern times we have gained numerous facts ABSENCE OF THE PERICARDIUM. 549 which aid in the recognition of pericardial diseases and especially in the study of adherent pericardium ; yet these advances belong not to history, but to the present day. Absence of the Pericardium. Baillie, Transact, of a Societ. for the Improv. of Med. and Chir. Knowl. Lond. 1793. I.—Breschet, Rep. d'anat. et de phys. path. I.— Wolf, Rust's Mag. Bd. 23. —Curling, Med. chir. trans. Vol. 22.— Otto, Selt. Beobachtg. Bd. II.—Baly, Lond. Med. Gaz. 1851.—Rokitansky, Handb. 2. Bd.—Powell, R. Douglass, Case of pneumothorax with congenital opening in the peric. Trans, of the Path. Soc. XX. p. 29.—P. Bert, Insuffisance du peric. Gaz. de Paris. 18G6. No. 33. Theilweiser Defect bei einem Hunde.—A. Weissbach, Angeborner Defect des Herzbeutels. Wiener med. Wochenschr. Aug. 26. 1868.— Virchow-Hirsch, Jahrb. f. 1869. I. S. 168. Absence of the pericardium occurs in ectopia cordis and is then generally only partial, and we find in that anomalous posi- tion of the heart an opening or fissure in the sac through which the heart protrudes. In other cases, the heart and the left lung may both lie in a single serous sac common to both ; in such cases the heart is covered by the visceral layer of the pericardium, and at the origin of the great vessels there are usually found rudimentary portions of the parietal layer in the shape of fringe- like reduplications. The latter condition gives rise to no symp- toms during life, as the case of Baty shows. Slight deficiencies in the pericardial sac are occasionally observed at autopsies. Formation of Diverticuli. Cmvrilhier, Anatom. path. Livr. 20. pi. 2.—Hart, Dubl. Journ. of Med. Sc. 1837, July.—Rokitansky, Handb. II. S. 232.— Luschka, Die Structur der serosen. Haute. S. 73.—Bristowe, Divertic. from the peric. Trans, of the Path. Soc. XX. p. 101. The formation of diverticuli is rarely observed ; the develop- ment of such hernia-like sacs is due to the outward pressure of fluid within the pericardium : portions of the fibrous layer yield and separate or become thin and allow the serous layer to pro- 550 BAUER.—DISEASES OF THE PERICARDIUM. trade. Most of tliese cases have a chronic development. In a case related by Cruveilhier the bulging was occasioned by the distention of the pericardial sac with blood, in consequence of rupture of the left ventricle. The size of the diverticuli which have been observed was usually small, yet one in a case related by Hart contained from three to four ounces of fluid. The open- ing of communication with the pericardial sac may be wide or narrow. Usually the formation of diverticuli is unrecognized, and only the pericardial effusion which caused it is made out. Yet we might conceive it to be possible that a large diverticulum, capable of containing three or four ounces if in a favorable position, might be accessible to physical investigation, even though it escape diagnosis. Tendinous Spots (Milk Spots). Bizot, Rech. sur le coeur etc. Mem. de la soc. med. d'observ. de Paris. Tom, I. 183G. p. 347.—J". Reid, Cyclop, of Anat. and Physiol. Vol. II. London. 1839. Art. "Heart" andi?. B. Todd, ibid. Art. "Abnormal conditions of the heart." —James Paget, On white spots on the surface of the heart. Med.-chirurg. Transact. II. S. V. Vol. London. 1840.—Hasse, Anat. Beschreibung der Krankheiten der Circulations- u. Respirationsorg. Leipzig. 1841. S. 142.— See, in addition, the various text-books on Path. Anat. and on Dis. of the Heart, especially that of Friedreich, Krankh des Herzens. Virchow's Path. u. Therapie. V. 2. We use the term tendinous spots or milk spots on the pericar- dium (macule tendinese or lactese, also insulse) to describe the circumscribed whitish cloudy appearances and thickenings of the pericardium, which are so frequently observed in the autop- sies on adults, that Baillie, Soemmering, and others believed that they were not of pathological origin. These are most frequently met with in people of advanced age, while in youth they are less frequently seen, and in children very rarely. They are oftener found in men than in women. Bizot has made a collection of autopsies in one hundred and fifty-six individuals, which in regard to age and sex gave the fol- lowing proportions: TENDINOUS SPOTS ; MILK SPOTS. 551 Men. From the 1st to the 17th year in 16 persons............... 0 cases. " " 18th " 39th " 24 " ............... 8 " " " 40th " 79th " 32 " ............... 23 " Women. From the 1st to the 22d year in 31 persons............... 0 cases. " " 23d " 39th " 23 " ............... 5 " " 40th " 89th " 30 " ............... 9 " Accordingly in one hundred and fifty-six individuals tendinous spots were found forty-five times. If an estimate were made from autopsies of adults only, the proportion would naturally be much greater. Bizot denies their occurrence in children altogether, which certainly is incor- rect (Foerster, Hodgkin). The tendinous spots are formed only exceptionally on the parietal layer of the pericardium ; most frequently they are on the visceral layer, and in by far the greater number of cases on the anterior face of the right ventricle, along the coronary arteries. Yet they do occur on other parts of the heart, and at the origin of the great vessels, either singly or in groups. These tendinous spots have no clinical importance whatever, since they are accompanied by no functional disturbance, and their presence cannot be recognized by any symptom during life.1 There is a certain interest attached to them, however, since some authors have regarded them as the remains of inflammatory processes, traces of antecedent pericarditis (Paget, Rokitansky, and others). Others again deny their inflammatory origin, and claim that they are simply fibrous thickenings, such as occur on serous membranes elsewhere, especially on the arachnoid. Bizot distinguishes two forms of tendinous spots, and considers one only the result of changes accompanying age; this form is by far the most frequent. The other rarer form is of inflammatory origin, and consists of granular or flat patches, opaque, whitish, and of a firm consistency, which may be pulled off, without tear- ing, from the serous layer, with which they are loosely connected. It cannot be denied that a circumscribed pericarditis with 1 It is alleged, however, that tendinous spots sometimes occasion a friction mur- mur ; but we could hardly believe that most tendinous spots were capable of produ- cing a friction sound, and observation supports that belief. 552 BAUER.—DISEASES OF THE PERICARDIUM. surrounding thickening of the serous coat may terminate in a " milk spot," but, in the majority of cases, tliese changes are to be considered not as inflammatory, but rather as circumscribed hyperplasias of connective tissue and scleroses. Thus, the change consists less in a new growth of connective-tissue fibres than in a consolidation of those already existing. It is not possible to lay down sharp lines of division between these processes and that which is truly inflammatory,' but in a clinical point of view it is important to remember that the formation of most of these spots is the result simply of a chronic hyperplastic process. It may be true, as Friedreich asserts, that these tendinous spots arise from a continual mechanical irrita- tion of the surface of the heart, and accordingly are most fre- quently found on those parts of the heart which, uncovered by lung tissue, are continually brought into contact with the more resisting portion of the thoracic wall. As opposed to the idea of the inflammatory origin of these milk spots, we might mention the fact that they are rarely accompanied by adhesions. Chambers found in one hundred and sixty such cases that only three times did adhesions exist simultaneously ; and Fried- reich confirms tliese proportions, as opposed to Paget. Inflammation of the Pericardium J. B. Morgagni, De sed. et causis morb. per anat. indag. lib. IT. cp. 16. 17. and in other parts of the work.—Riolanus, Ench. anat. path. 1. III. c. 4.—Holler, Ele- ment, phys. Vol. I. p. 285 and Add. ad elem phys. p. 128.—Senac, De la struct., de Tact, et des malad. du cceur. Paris. 1749.—De Haen, Rat. med. Tom. XIV. p. 30.—Trecourt, Chirurg. Abhandl. u. Wahrnehm. aus dem Franzos. Leipzig. 1777.—Romero, Diet. des. sc. m£d. Tom. XL 1819.—Stoerk, Annal. med. Vol. II. p. 232, 264.— Watson, Philos. Trans. 1777.—Savary, Sur la peri- card, aigue. Diss. Paris. 1819.—J. G. Walter, Observ. anat. p. 63 ; Mus. anat. Vol. I. p. 148.—Portal, M6m. sur plus. mal. Tom IV. u. Cours d'anatomie med. Tom. III. p. 24.—Lemazurier, D. sur la pgricardite. Paris. 1810.—J. C. Boullier, D. sur la difficulty du diagnostic de la pericard. Paris. 1812.—Roux, Collect. quaedam de cardit. exsud. Lips. 1819.—Hubert, Diet, de med. Ed. 2. Art, See Rindjleisch, Patholog. Gewebelehre. PERICARDITIS.—BIBLIOGRAPHY. 553 Pericarditis.—C. C. Diergardt, De pericard. acut. diag. Bonn. 1828.—Collin, De divers, meth. d'exploration de la poit. Deutsch von Bourel. Koln. 1828. —Louis, Mem. sur la p6ric. Revue med. Janvier, 1824; Rech. anat. path. Paris, 1826.—Andral, Clin. mod. Tom. I. u. Tom. III.—J. Abercrombie, Trans. of the med. chir. Soc. of Edinb. Vol. I.—Bouillaud, Art. " Pericardite " in Diet, de Med. et Chirurg, 1834; Rech. sur le rhum. artic. aigue. Paris. 1836.— Sander, Hufeland's Journ. Bd. 51. 1820.—Seidlitz, Ueber Pericard. exsud. sang. Ilecker's Ann. II. 1835.—Desclaux, Ess. sur la peric. aigue. These. Paris. 1835. Arch. gen. denied. 1836.—J. P. Latham, Lond, Med, Gaz. Vol. III. p. 209.— Adams, Dubl. Hosp. Rep. Vol. IV.—Hache, Mem sur la peric. Arch. gen. de med. II. Ser. Tom. IX. Paris, 1835.—Brissault, Ess. sur la peric. etc. Strassbourg 1826.—Stokes, Lond. Med. and Surg. Journ. Sept, Oct. Dec. 18ZZ.—Stiebel, Monog. card, et pericard. acut. etc. Franc, ad M. 1828.—R. Mayne, Dubl. Journ. Vol. VII. 1835. May u, Schmidt's Jahrb. Suppl. I.—Rayer, Arch. gen. de med. Tom. 1. p. 521.— Hughes, Guy's Hosp. Rep. 1836. No. 1; Schmidt's Jahrb. Bd. XVI. Lond. Med. Gaz. Vol. XIX. Schmidt's Jahrb. Bd. XVII.—J. Watson, Lond. Med. Gaz. 1836. July.— Roots, St. Thomas's Hosp. Rep. No. 4. June, 1836. Lond. Med. Gaz. 1836. Nov.—R. W. Smith, Dubl. Journ. Vol. IX. p. 418.— Heyfelder, Heidelb. klin. Annal. X. 1834. Schmidt's Jahrb. Suppl. I. Stud. im Gebiete der Heilwissensch. Bd. I. S. 208.—Richter, Preuss. Vereinsz. 1834. No. 47.—G. Corfe, Lond. Med. Gaz. 1835. June.—Maisonneuve, Arch. gen. 1834. Apr.—Ebers, Hufeland's Journ. St. 7. 1837.—Bright, Cases of spasmodic disease accompanying affect, of the pericard. Med. chirurg. trans. Vol. XXII. Lond. 1839.—Karaicajeff. Preuss. Vereinszeit. No. 52. 1840.— Taylor, Lond. med. surg. trans. Vol. XXVIII. 1845. Med. Tim. Vol. XXI. 1850.— Aran, Arch. gen. 1844. Avril u. Gaz. des Hopit. No. 38. 1858.—Brockmann, Holscher's Annal. Jahr. V. H. 3. 4.—Roger, Arch, fur phys. Heilk. V. Bd. 1846.—Kyber, Bemer- kungen iiber den Morb. cardiac. Med. Zeitg. Russlands. 1847. Nos. 20-25.— Schwank, De haemoperic. scorbut. Diss. Dorpat. 1847.—Sibson, On pericarditis. Lond. Med. Journ. Oct. 1849.—Chambers, Med. chirurg. Rev. Oct. 1853.—Lalor, Dubl. Quart. Journ. of Med. Sc. Vol. XIII. Sept. 1852.—Eisenmann, Die Familie rheuma. Bd. III. S. 72.—Civati, D. de pericard. Ticin. 1841.—Skodm, Oesterr. medic. Jahrb. 1841. Marz.—Graves, A syst. of clinic, med. Dubl. 1843. Clinic, lectures. Lond. u. Dubl. 1848.—Skoda und Kolletschka, Ueber Pericar- ditis in path, und diagnostischer Beziehung. Oesterr. med. Jahrb. N. F. XIX. 1839.—King Wilkinson, Lancet. 1845. Nov.—Barthez et Rilliet, Mai. des enf. I. —Baillie, Engravings, fasc. 1. pi. 1.—Albers, Atlas III. t. 1. 2; Erlauterungen III.—Cruveilhier, Anat. path. livr. 16. pi. 2. livr. 30. pi. 4. livr. 40. pi. 4.— Froriep, Klin. Kupfertafel. t. 61.— Virchow, Acute Fettmetamorphose des Herzfl. bei Pericarditis, dessen Arch. XIII. 1858.—Gerhardt, Zur Casuistik der Herz- krankh. Wiirzb. med. Zeitschr. II. 1861. S. 136. und Ueber einige Formen der Herzdampfung. Prager. Viertelj. Bd. 84. 1864.—Duchek, Zur Aetiologie der Pericard. Wien. med. Wochenschr. No. 15. 1859. und Klinische Vortrage iiber 554 BAUER.—DISEASES OF THE PERICARDIUM. Herzkrankh. Allg. Wien. med. Zeitung. Nos. 24-32. 1862.—Ch. Hirsch, Klin- ische Fragm. 2. Abth. Konigsberg. 1858.—Gairdner, On pericarditis. Edinb. Med Journ. April, 1859. p. 904. Febr. 1860. p. 736. January, 1861. p. 626.— Oppolzer, Ueber Pericarditis. Allgem. Wien. med. Zeitung. No. 44. et seq. 1861. und Spitalzeitung No. 19. 1862.—Leudet, Recherch. auat. path, et cliniques sur les peric. second. Arch. gen. de med. Juil. 1862.—Kirkes, On peric. conseq, on pyaemia. Med. Tim. and Gaz. Oct. Nov. 1862.—Kirby, Rep. of a fatal case, etc. Lancet. Jan. 1860.—F. Roth, Zur Casuistik der Herzbeutelentziindung. Wiirzb. med. Zeitschr. in. 1. 1863.—Kaulich, Krankh. der Kreislaufsorgane. Beob. auf der Klinik von Prof. Jakschzu. Prag, wahrend 1857-59. Prager Viertelj. LXXIII. 1862.—Cejka, Aus dessen lit. Nachlasse. Prag. Viertelj. 1. 1863.— W. D. Moore, Sur un cas sing, de peric. Gaz. med. de Paris. 18G3. No, 31. u. Dubl. Med. Press. 1862.—Kerschensteiner, Ueber Pericard im kindl. Alter. Bayr. arztl. Intelligenzbl. 2. 1863.—Radcliffe, Extens. pyoperic. and cmp. etc. Lancet. Aug. 1863.—Ormerod, On rheumatic and non-rheumatic pericarditis. Med. chirurg. trans. Vol. XXXVI. Lond. 1853. and Med. Tim. and Gaz. Aug. 1864.—Trousseau et Lassegue, De la paracentese du peric. Arch. gen. de med. Nov. 1854.— Gimzburg, Dessen Zeitschr. VI. H. 2 u. 3. 1855.—Bamberger, Beitr. zur Phys. u. Path, des Herzens. Virch. Arch. IX. 1856. S. 348.— Vernay, Sur la ponct. du peric. Gaz. hebd. No. 45. 1856.—Hamernjk, Grundziige der Phys. u. Path, des Herzbeutels. Prag. 1864.—Mettenheimer, Ueber pericard. Reibungs- i gerausche ohne Pericarditis. Arch, fiir wissensch. Heilk. 1865. No. VI.— Gueneau de Mussy, De cert. sign, de la peric. Gaz. des Hop. 1865. No. 49.— Armand Debest de Lacrousille, De la peric. hemorrhg. Union med. 1865. 1.— Traube, Ges. Beitrage. II.— Thore, Arch, gener. 1856. Fevr. — Fetters, Prager Viertelj. 50. Bd.—Law, Dubl. Quart. Journ. 1856. Aug.—H. Kennedy, Edinb. Med. Journ. No. 1858.—Page, Haemotoperic. and compl. fatty degen. of the heart, sudden death. Lancet. 1863.—R. E. Thompson, On rheumat. pericard. St. George's Hosp. Rep. IV. pp. 31-44.—rllambursin, Bull, de l'acad. de med. Belg. 1870. IV. p. 990. Ibid. p. 930—Of the different treatises and text-books on Diseases of the Heart, consult, in particular, Bamberger, Duchek, Fried- reich, 1. c. Pathogenesis and Etiology. Inflammation of the pericardium may occur both on the visceral and on the parietal layer, and throughout its whole extent, or the process may attack only single portions of the surface of the heart. Accordingly we distinguish two varieties, viz., diffuse and circumscribed pericarditis. In most cases the whole pericardium is affected. The existence of the opposite condition is proved, however, if we include the " milk spots " amongst inflammatory PERICARDITIS. —ETIOLOGY. 555 processes. Still it will be difficult to lay down an accurate numerical proportion between the two forms, since during life an opinion concerning the extent of the inflammation in many cases will only be an approximate one, and since a circum- scribed pericarditis may run its course without any symptoms. Thompson found iu rheumatic pericarditis a proportion of 94 to 38. The circumscribed inflammation may occur on any part of the heart; its seat of election, however, is at the base, at the origin of the great vessels. As regards the course of the disease, we can divide them into acute and chronic cases, without, however, making a sharp boundary line, or a decided distinction between the two cate- gories. A further subdivision is based on the quantity and character of the exudation ; thus, according to its nature we speak of a pericarditis as fibrinous, serofibrinous, hemorrhagic, or purulent. Inflammation of the pericardium rarely attacks a man in previous good health in a primary idiopathic manner, and even amongst those cases which are apparently idiopathic doubtless many, as von Bamberger has likewise remarked, are secondary, and the original disorder has escaped observation. Perhaps there are sometimes pathological changes in the mus- cular tissue of the heart itself which lead to a secondary pericarditis. Here we might readily be deceived. Inflammations of trau- matic origin are generally reckoned amongst the idiopathic cases, and of these numerous examples are found in the literature of the subject, of the most various kinds, according to the charac- ter of the injury received. Thus, cases are found depending upon a blow or jar against the breast, upon crushing of the thorax, following upon penetrating wounds, bullet wounds, and the penetration of various foreign bodies. A wonderful case of this kind was observed by Buist, and is cited by Friedreich: a pericarditis was caused by swallowing a set of false teeth, which remained fast in the oesophagus, and the gold rim had bored its way into the right portion of the pericardium posteriorly. With regard to the other causes of primary pericarditis we have no accurate information. Catching cold is sometimes as- 556 BAUER.—DISEASES OF THE PERICARDIUM. signed as a cause, still we can hardly satisfy ourselves with this explanation. Some of the patients of this kind whom I have observed were decided drinkers, others were living under circum- stances of much privation and exhaustion. All statements agree as to the inf requency of primary pericarditis. For example, out of 89 cases of pericarditis, Duchek observed only one case; Bamberger found only 5 out of 63 cases, and of these one was traumatic. Out of about 3,000 patients, which is the usual number in each year in the medical division at Munich, I have seen yearly two or three cases of spontaneous pericarditis. The secondary affection, on the other hand, as Corvisart taught us long ago, is a very frequent disease. Of the diseased conditions with which pericarditis is most frequently associated, polyarthritis rheumatica certainly holds the first place, although up to the present time we have not been able to make the con- nection clear between inflammation of the pericardium and articular rheumatism. The dependence of pericarditis upon rheumatism has been recognized since the time of Pitcairn (1788). The statements regarding the frequency of this compli* cation of articular rheumatism differ within very wide limits (see Senator's article in one of the later volumes of this cyclopaedia). Certainly the figures of Bouillaud, Williams, and others concerning the frequency of heart affections, and particularly pericarditis, in the course of this disease are far too high, for, according to them, pericarditis occurs in half the cases, or even more. Tliese exaggerated statements depend partly upon erroneous diagnoses. It cannot be denied that the frequency of the occurrence of pericarditis in the course of rheumatism is not always the same, but I think we should be near the truth if we should say that from 16 to 20 per cent, of the cases are complicated by pericarditis (Leudet, Chambers, Duchek, Thompson, Lebert, and others). The relative percentages of cases of pericarditis of rheumatic origin, and those in which the pericarditis was due to other causes, naturally vary very greatly; thus Ormerod observed 71.7 per cent., and Chambers only 13 per cent of cases of peri- carditis associated with rheumatism, and the statistics of others hold a middle place between these two extremes; von Bamberger asserts that about 30 per cent, are of rheumatic origin. I believe that we cannot lay down any percentage which will hold everywhere, since rheumatism in a severe form depends, in its frequency, upon local causes. Wherein the cases of articular rheumatism, complicated by pericarditis, differ otherwise from cases without such complica- tion, we do not certainly know. This complication certainly oc- PERICARDITIS. —ETIOLOGY. 557 curs more frequently in the course of severe cases; and yet this is only the rule, and the pericardium may be affected in those which are only very moderately severe. On the other hand, the number of joints affected bears no relation to the frequency of pericarditis, and much less does the affection of certain joints, particularly those of the upper extremities, have any influence. So, likewise, the effect which repeated attacks of rheumatism will have upon the tendency to pericardial affections is not surely established. According to Thompson, the first attack is the one most frequently accompanied by pericarditis. Pericardial inflam- mation does not occur in chronic articular rheumatism, nor in rheumatic inflammation of a single joint, nor in muscular rheu- matism, nor in gout. The occurrence of pericarditis has been observed most fre- quently between the sixth and fourteenth days, or between the fourth and tenth, yet it may occur as well later as earlier in the disease, and there are well-authenticated cases in which the pericardial affection preceded the articular trouble. A marked predisposition to secondary pericarditis is an accompaniment of chronic diseases of the kidneys, and specially of fatty degenera- tion of these organs, and stands in the same class with the increased tendency to peritonitis and pleuritis, which are sequelae of these affections. For the causal connection between tliese secondary troubles and the primary disorder we must refer to what has been said elsewhere concerning the inflammation of serous membranes as a sequel of Bright's disease (see the chapters on that subject in this cyclopaedia). On this point, also, the statistics of various observers are greatly at variance, which may here be explained by local variations and partly also by insufficient accuracy in the conception of the meaning of Bright's disease. The frequency of the occurrence of chronic renal affections is doubtless very different in different localities, and accordingly the number of cases of pericarditis secondary to such diseases must also be very varied. Moreover, it is stated that, in a given number of cases, the tendency to pericarditis is not everywhere the same. Frerichs observed pericarditis thirteen times in 292 cases, and Rosenstein eight times in 114 cases.1 1 Rosenstein, Krankheiten der Nieren, p. 197. 558- BAUER.—DISEASES OF THE PERICARDIUM. Pericarditis also occurs quite frequently in the course of pyaemic processes and especially in puerperal pyaemia; yet in these diseases pericarditis falls far behind pleuritis in the fre- quency of its development. The method of its development is the same as in the inflammations of other serous tissues which so frequently follow pyaemic infection. The connection described by Kirkes, between pyaemic pericarditis and pyaemic abscesses in the myocardium, doubtless holds chiefly for diphtheritic endocarditis. Pericarditis occurs occasionally also in the course of other acute infective diseases, as in scarlatina—according to Gendrin especially at the time of desquamation1—in measles, variola, exanthematous typhus, also in severe malarial fevers, in cholera, etc.; very rarely in typhus abdominalis (typhoid), erysipelas, and others. Among chronic constitutional diseases, those with the so-called hemorrhagic diathesis are quite frequently complicated by peri- cardial inflammations ; for instance, the morbus maculosus, espe- cially scorbutus, as was accurately recognized by Seidlitz and Kyber, in which the exudations have a specially hemorrhagic appearance (pericarditis exsudatoria sanguinolenta, pericarditis scorbutica). Tuberculosis may be accompanied by pericardial in- flammations of various kinds ; it may be simply fibrinous, or sero- fibrinous, hemorrhagic or tubercular in character ; exceptionally it may happen that a cavern in the lung perforates the pericardi- um and pours its contents into the sac. Pericarditis, however, is not a frequent accompaniment of tuberculosis. Rarely pericardi- tis occurs as a sequel of cancerous cachexia ; and here it may be either a simple inflammatory process or development of the new growth upon the serous membrane. In tuberculosis of the lungs we must explain some of the secondary pericardial inflammations, by believing that, from the foci of inflammation in the neighbor- hood, inflammatory products and irritants find their way through the lymph channels into the pericardium. In the same way all other inflammatory processes in the vicinity of the pericardium 1 Snow believed that the pericarditis in scarlatina was caused by the trouble with the kidneys. In two cases of pericarditis accompanying scarlatina which I saw, there were rheumatic inflammations of the joints at the same time, and in one case, before the disappearance of the eruption, without any accompanying trouble in the kidneys. PERICARDITIS.—ETIOLOGY. 559 may involve it by sympathy. This is true of acute and chronic pneumonias and pleurisies, especially when the exudation is purulent; effusions on the left side more frequently lead to peri- carditis, but those on the right also cause it; pneumonia and pleurisy, after polyarthritis rheumatica, are doubtless the most frequent of the diseases giving rise to pericarditis. In rare cases empyema breaks through into the pericardial sac. The earlier observers, as Senac, Morgagni, and others, had seen most of the cases of pericarditis occurring as a sequel of pleuritis. Since the time of Bouillaud acute articular rheumatism has been considered the most frequent cause. Duchek clings to the old impression; but this sequence will be sustained only, as I believe, by statistics of the fatal cases of pericarditis alone. The processes which are comparatively rare in the thorax, such as ulcerations and new growths in the oesophagus, the bronchial glands, the mediastinum, and the lungs, caries of the vertebrae and the ribs, may occasionally cause inflammation of the pericardium, either by the extension of the inflammatory process or by ulceration of the pericardium—in the latter case with the formation of a so-called internal fistula of the pericar- dium. Processes going on below the diaphragm, such as peri- toneal inflammations (aside from the infective form), encapsulated abdominal exudations, perihepatitis, abscesses in the liver and spleen, echinococci, gastric ulcers, and new growths in the abdo- men, may lead to pericarditis, with or without perforation of the diaphragm. All serous membranes are intimately connected with the organs which they surround, and take part in the diseased processes which affect them. This is true also of the pericardium, and all the various diseases of the heart may give rise to peri- carditis ; more especially is this true, however, of myocarditis and the degeneration of the muscular tissue which is observed particularly in hypertrophied hearts, next of abscess of the mus- cular tissue, endocarditis, and aneurisms, especially when they lie within the pericardium or press against it. With the list already given, we have not exhausted all the diseases which at times are complicated by pericarditis ; but cases arising otherwise than as above are exceptional or have no direct dependence upon the original disease. 560 BAUER.—DISEASES OF THE PERICARDIUM. If we consider the absolute frequency of pericarditis, it will be clear that the numerical relation to the total number of indi- viduals sick with diseases of all kinds and to the total mortality from all causes cannot everywhere and at all times be the same, and this variation will be occasioned hy the varying frequency of the chief primary diseases on which it depends. The accounts of an endemic pericarditis, such as are given by Trecourt, Hubert, and Lalor, are to be explained by the increased frequency, which sometimes is seen, of those diseases to which it is secondary. Thus, in the first two of the writers above mentioned who observed it, doubtless the primary disease was pleuro pneu- monia, which frequently appeared in the troops acting as a garrison for fortifica- tions, and with it was associated a purulent pericarditis. Just as in acute rheumatism, so in these other diseases it is difficult to recognize any conditions which will explain the occurrence of pericarditis in one series of cases, while in other cases, under apparently similar circumstances, it does not occur. Pericarditis occurs most frequently in middle life, and oftener in the male than in the female sex, and for the reason that the primary disorders which give rise to it show the same prefer- ence. In children inflammation of the pericardium is rare, and, according to Virchow, most frequently associated with pneumonia. Although the greatest number of cases of peri- carditis occurs in middle life, yet the statement of Willigkisnot at variance with this fact, viz., that the disposition to this dis- ease amongst very old people is considerable, when we compare them with a similar number of individuals at other periods. This statistical observation of Willigk has certainly been called in question, but has not been disproved. The greatest frequency of pericarditis during the coldest months in the year is due likewise to the great prevalence at that time of the primary disorders. Formerly and up to the close of the last century pericarditis was considered a rare disease ; since then it has been proved that it is of quite frequent occurrence. The absolute numerical pro- portion to the total number of cases of sickness or to the total mortality cannot be easily established, since its frequency is due to circumstances which are not everywhere the same, as has already been remarked. PERICARDITIS.—PATHOLOGICAL ANATOMY. 561 In giving the statistics of deaths the proportion will be varied also according as the " milk spots " are included in the cases of pericarditis or not. Usually they have been included. Duchek found 15.1 per cent.; Willigk, 14.1 per cent.; Chambers, 16.2 per cent. ; Taylor, 12.5 per cent. Pathological Anatomy. The anatomical processes which accompany pericarditis are essentially the same as are observed in inflammation of other serous membranes, especially that of the pleura. The visceral and parietal layers of the pericardium are both affected by the inflammatory changes ; but frequently the process is more pro- nounced on the visceral than on the parietal portion, and the degree of the morbid process is not the same in all parts. The characteristics of the inflammation are hyperaemia of the serous layer and sub-serous tissue, with parenchymatous swelling, formation of a fibrinous exudation on the surface of the membrane, and the outpouring of a fluid effusion into the pericardial sac, varying in quantity and appearance. In the lower grades of the hyperaemia the injected vessels form a fine network, and in the higher grades the membrane is of a uniform dark-red color. With the hyperaemia, small spots are frequently found where blood has escaped, especially round the newly formed vessels. In the pericarditis of cachectic individuals and those of advanced age, the hyperaemia is ordinarily less in- tense. In the further course of the process the hyperaemia gen- erally subsides, or at least is covered by the fibrinous exudation. In the first stage of the hyperaemic condition the dull sheen of the serous coat is replaced by a cloudy and velvety appearance. The hyperaemic stage does not last long, perhaps only a few hours, and then begins the fibrinous exudation upon the free sur- faces, and most frequently at the origin of the great vessels. This exudation varies greatly in quantity and external appear- ances, in different cases, according to the duration of the inflam- matory process. It may be a delicate, thin covering, like a bloom, only at single places on the surface, especially on the visceral portion, or it may cover the whole heart, and the parietal layer as well, as a pretty thick network or shaggy bark. Frequently VOL. VI.—36 562 BAUER.—DISEASES OF THE PERICARDIUM. long papillae stretch across from the visceral to the parietal layer, and may form firm partitions in the cavity. A perfectly smooth surface on the fibrinous exudation, like croup membrane, is rarely observed; most frequently it has an areolar texture. This varied appearance of the irregular surface has given rise to various figurative names, such as cor vil- losum, or tomentosum and hirsutum, and, in the German, Zottenherz, Mantelherz, etc. Occasionally the comparison made by Laennec is very striking, who said it looked as if two flat surfaces had been spread with butter and pressed together, and then pulled apart. The fibrinous exudation has usually a whitish yellow or red- dish yellow color, is of pretty firm consistency, and on pulling it apart we find it very elastic. Frequently we find numerous hemorrhagic points in the layers of exudation, and after a short time it is with difficulty that they can be separated from the serous membrane, for the new-formation of vessels takes place rapidly. The membranes consist of fibrine and numerous cell elements. The upper layer of a fresh fibrinous membrane is usually almost lacking in cell elements ; but deeper, near the serous layer, the cells are very numerous. We must consider them as wanderers from the endothelium, or, as having escaped from the vessels. In other cases the exudation is less firm, sometimes infiltrated with serum, and occasionally it is soft, boggy, or crumbling, or may have the consistency of jelly. This results from the admix- ture of a great number of cell elements (pus corpuscles) and from the molecular destruction of the exudation. The quantity of fluid which is poured out into the sac is very varied ; it may be so small that the name dry, or fibrinous peri- carditis, though not actually, is comparatively correct; in cases of this kind we frequently find the layers of the pericardium loosely adherent. Occasionally the connection is formed by a network scaffolding of fibrinous strings, the meshes of which are filled with serum. In extreme cases the fluid may amount to a quart or more. As the body lies at an autopsy, we usually find most of the fluid at the anterior and upper part of the sac, since the heart, which is the heavier, falls backwards and downwards. This position naturally may be variously changed by adhesions. PERICARDITIS.—PATHOLOGICAL ANATOMY. 563 As a result of the exudation, the complementary space in the sac will first be filled with the fluid ;* in more extensive effusions the sac will be more enormously distended, and, indeed, there may be thinning of its walls, but more frequently in inflamma- tory effusions there is thickening and increase in volume, for the texture of the pericardium is involved in the inflammatory processes on its free surface. When the disease has a longer duration, numerous connective tissue corpuscles are formed in the parenchyma of the serous layer, and more abundantly the closer you come to the free surface of the same. At the same time the whole tissue is swollen, loosened, and thickened. The color of the fluid exuded is bright yellow and trans- parent or greenish; in other cases it is brownish in various shades, deepening actually to a hemorrhagic appearance, or finally to that of pure blood. In consequence of these hemor- rhages, which generally occur from the newly-formed vessels, the fibrinous layers are stained of a brown or reddish color. While a slight admixture of blood is not rare and has no particular significance, distinct hemorrhagic exudations, as a rule, are found only in individuals with some constitutional dys- crasia, as in tuberculosis, and also in the course of acute general diseases. Yet hemorrhagic pericarditis does occur in healthy people, especially in the chronic forms, and I have seen most beautiful examples of it in individuals suffering from chronic alcohol intoxication. Hemorrhagic exudations are particularly marked in those diseases which cause hemorrhages elsewhere in the body, such as scurvy and morbus maculosus. In regions where scurvy prevails, these cases are often seen associated with extensive hemorrhagic exudations, and have been described by Seidlitz as pericarditis exsudatoria sanguinolenta, and by Kyber as pericarditis scorbutica. If the effused fluid does not contain blood, it is either entirely clear or little flakes of fibrine are seen suspended in it, of the same appearance as the layers which line the pericardium. In other 1 According to Rudinger (Topograph. Anatomie, Abth. 1 u. 2 S. 49) the sac is larger than its contents require. Accordingly, there is a complementary space into which the heart doubtless falls at first, while the fluid collects at the upper part near the base. 564 BAUER.—DISEASES OF THE PERICARDIUM. cases the fluid is opalescent from its richness in cell elements. When they are still more abundant the fluid becomes cloudy, opaque, and of all grades of density up to a marked purulent character. While in other serous membranes, particularly in the peri- toneum, the fluid often has a purulent character from the first; in the pericardium this, doubtless, is not the case—here the pus is always secondary. The causes which in some cases lead to the formation of pus are probably mani- fold, and are not easily defined. Yet certain conditions should be mentioned to which a certain influence may be ascribed in the more abundant cell growth which is sometimes observed. Among these may be reckoned the constitution of the patient, the nature of the primary causal disease, and also the deposit of inflamma- tory products upon the surface of the pericardium. In the last-named condition the extensive formation of new blood-vessels in the pseudo-membrane doubtless favors the development of pus. The formation of pus does not ordinarily lead to a purulent destruction of the serous membrane, but its surface becomes like that of the granulating surface of a wound (Rindfleisch). Yet in exceptional cases purulent destruction and loss of substance do occur, and it is by means of these processes that perforation of the pericardium has been observed. A case of this kind was described by Wyss, in which, after wearing away the rib, a fistulous opening was established and remained patent for years, until finally the patient was carried off by an attack of pericarditis. A foul and ichorous condition of the exudation in the pericardium is very rarely seen; cases of this kind are generally associated with destruction by gan- grenous or carcinomatous processes going on in the neighboring parts, e. g., proceeding from the oesophagus; entrance of air into the pericardial sac may also cause a foul condition of its contents. This condition has also been observed in cases where no local cause could be found sufficient to explain it, and when it had to be referred to a general septic condition of the system. We might well doubt whether in the absence of any of these or any similar causes we could attribute it to spontaneous decomposition. From what has been said above, we may divide the exudations in pericarditis into those of a serous, sero-fibrinous, hemor- rhagic, and purulent (and in rare cases ichorous) character. PERICARDITIS.—PATHOLOGICAL ANATOMY. 565 The methods of progress toward cure are analogous to those in inflammations of other serous membranes. Thin, serous effusions are absorbed. Doubtless, also, fibrinous exudations may be completely absorbed, so that there is an entire "resti- tutio ad integrum," or there remains at most a thickening, of various degrees, of the tissue of the pericardium. This favorable result depends upon the thickness and extent of the fibrinous deposit, and especially upon the length of duration of the process. In those cases in which the fibrinous deposit is only partial and not very abundant, as we must believe it to be in many cases of pericarditis secondary to polyarthritis rheumatica, we find at the autopsy only very slight remains, or none at all, of the pericarditis which has occurred. The absorption of the fibrinous exudation takes place through a fatty molecular destruction. Moreover, it is probable that loose adhesions, by means of connective tissue, may subsequently be broken up, for the continual movements of the heart pull and stretch the newly-formed membranes, and, moreover, beside this mechanical violence, the circulation of the blood in the newly-formed vessels must be considerably interfered with by the movements of the heart. Just this constant and yielding friction of the parts is the chief reason why permanent firm adhesions in the pericardium are more rare than in other serous membranes. In those cases also in which, from the inflammatory process, new growth of connective tissue and adhesions of the pericardial layers take place, the fibrinous exudation takes no part in the process, but is absorbed after fatty degeneration. The organization of connective tissue results from the cells present in the exudation, and in very severe forms of inflamma- tion the tissue of the pericardium itself assists in the growth. The new-formation of connective tissue may occur in very various extent and arrangement. Besides superficial fibrous thickenings,1 we find irregular, knob-like projections or peduncu- 1 As a rule, the fibrous thickenings due to previous inflammation may be distin- guished from tendinous spots, especially by their greater thickness and extent, by their irregular distribution, and by the usual coexistence of adhesions. Often, however, the distinction is scarcely possible. 566 BAUER.—DISEASES OF THE PERICARDIUM. late outgrowths, which may even be found lying free in the pericardial sac ; also bands, either stretched to a thready thin- ness or of considerable thickness, up to a finger's-breadth, ex- tending from one layer to the other. In other instances we find the two layers adherent in circumscribed spots, or throughout their whole extent, by means of connective tissue, which is sometimes loose and at other times very dense. In the latter event we find the heart grown fast within a dense fibrous case, the two original layers of which can no longer be distinguished or separated. Calcification also occurs in the form of isolated concrements, and in rare cases the whole heart may become en- closed in a very hard calcareous capsule. Even hemorrhagic exudations may be absorbed, and the reason why such cases commonly prove fatal does not lie in the admixture of blood in the pericardial effusion, but must be sought for in those constitutional conditions which usually determine the hemorrhagic character of the exudation. Only in cases in which the admixture of blood is very abundant, so that the fluid looks like pure blood, can this occurrence of itself occasion death. Purulent exudations may likewise, in exceptional cases, end in recovery, the purulent effusion becoming thickened and the cells undergoing fatty metamorphosis, while the serous layers become adherent. It may then happen that these thickened masses become perfectly encapsulated. We find spaces between the adherent layers filled with a yellowish-white paste, made up of fatty or, together with these, calcareous molecules.1 The changes just described usually follow a more or less acute course to a definitive result. Cases are observed, however, in which an acute stage passes into chronic inflammation, but it is rare that we can assign to a simple pericarditis a chronic char- acter from the beginning. Cases of the last-named sort, which are occasionally to be observed in aged persons, are now and then distinguished by the excessively serous or even blood-tinged character of the effusion, and by the slight amount of fibrous 1 See the representation in Thierfelder, Atl. der path. Histolog. 4 Lfg., T. XX Fig. 3. PERICARDITIS.—PATHOLOGICAL ANATOMY. 567 exudation. Very likely there was in these cases primarily a transudation, to which inflammation was subsequently added. When chronic pericarditis follows an acute attack, we find thickenings and adhesions, whilst the fluid effusion is not all or only imperfectly absorbed. The effusion shows fluctuations, its amount increasing and diminishing by turns, fresh deposits of fibrine take place, hemorrhagic admixtures occur, or the exuda- tion takes on a purulent character. Such cases generally end in death. Circumscribed pericarditis is found, as a rule, upon the vis- ceral layer, and particularly at the origin of the aorta and pul- monary artery. It sometimes extends to the coats of these ves- sels, as far as they are covered by the pericardium, and gives rise to callosities, which even involve the middle coat. In this way pericarditis may be the cause, or at least a predisposing cause, of aortic aneurism. The changes in the muscular structure, which very com- monly occur in the course of acute and chronic pericarditis, and which must be looked upon as directly connected therewith, are of great importance. There are but few thorough observations in regard to the frequency with which pericarditis gives rise to such lesions ; according to Wagner, fatty change in the cardiac substance was found in seventeen out of thirty-five cases.1 Very likely this proportion is too low ; but certainly if we take into account not only fatty degeneration, but the inflammatory and degenerative processes of all sorts which may affect the cardiac muscle in the course of pericarditis, we find them, in various degrees of extent and intensity, in a great number of cases. The intensity and area of the inflammation of the pericardium, the character of the exudation, and, above all, the duration of the disease, are essential elements in the causation of changes in the muscular tissue. Myocarditic lesions are more frequently met with in hemorrhagic and purulent than in other conditions of the exudation, and in chronic cases they are prob- ably always present. Virchow believes that the occurrence of 1 Compare Schroetter, Myocarditis and Fatty Degeneration, p. 224 et seq., of volume. 568 BAUER.—DISEASES OF THE PERICARDIUM. muscular affections is favored by the strain, or increased work thrown upon the heart, particularly by the high fever. The view has also been expressed, that the pressure of the exudation impedes the normal distribution of blood to the substance of the heart, and that by means of this disturbance of the circulation the occurrence of degenerative changes is occasioned. In view of the importance of the serous membranes to those organs which they enclose, there is nothing surprising in the frequent occurrence of inflammatory and degenerative changes in the muscular structure of the heart in consequence of inflammations of the pericardium. The influence exerted by affections of the muscular structure of the heart upon the symptoms and course of pericarditis was pointed out by Stokes. Virchow has shown, by several examples, how high a degree of fatty degeneration may occur, even in cases of a wholly acute character. The changes may affect the cardiac muscle as a whole, but, as a rule, they are most clearly marked in those layers which are in immediate contact with the pericardium, so that therefore an advance of the process from without inwards is most strikingly manifest. The condition of fatty degeneration of the heart in connection with pericarditis has been thus described by Virchow: The surface of the pericardium was very rough with layers of fibrine. The substance of the heart throughout seemed flabby, pale, and somewhat spotted. Beneath the whole extent of the pericardium the outermost muscular layer had assumed a cloudy, pale-yellow appearance. This layer was from one to two lines in thickness, and within it were groups of primitive bundles in such an extreme condition of fatty metamorphosis that their internal structure could no longer be made out, even in the slightest degree. In the deeper layers this metamorphosis gradually decreased, but in no part of the muscular sub- stance of the heart was the interior of the primitive bundles entirely free from fat granules. Towards the surface, layers of proliferating connective tissue were met with, which extended into the thickened pericardium and the visible fibrinous layer, and which were thickly strewn with numerous masses of nuclei and cells, closely crowded together and in the act of subdividing. The best-marked cases of fatty degeneration answer to this description of Virchow's. Besides fatty degeneration, the other well-known acute and chronic disturbances of nutrition may affect the cardiac muscle in consequence of pericarditis. This is in part due immediately to anatomical conditions, and in part to sequelae. Thus, a peri- PERICARDITIS.—PATHOLOGICAL ANATOMY. 569 carditis may result in dilatation with consecutive hypertrophy of the whole heart or of an individual part, and this takes place with- out any obstruction to the current of blood, but merely by reason of the diminished impelling power and capacity for resistance on the part of the cardiac muscle as the result of preceding myo- carditic changes. The so-called abscesses or purulent softening of the muscular substance are rare.1 Some of these changes in the heart muscle are capable of repair; they may end with hypertrophy, but they may also assume a chronic course, with further extension. The latter is seen in adhesions of the pericardial layers, in which event the muscular substance becomes highly shrunken and atrophic, what remains of it being in a condition of connective-tissue or fatty degeneration. From the pericardium the inflammatory process may be prop- agated to the endocardium, as Desclaux has shown by experi- ment; acute endocarditis was developed in animals within a short time after an artificially induced pericarditis. As a matter of course, it is in but few cases that we can determine the depend- ence of an endocarditis upon a pre-existing pericarditis, since generally one and the same cause is capable of producing inflam- mation of both membranes. As a rule, the fibrous \nyer of the parietal pericardium does not share in the inflammatory process, but there are cases, par- ticularly of chronic pericarditis, in which the fibrous pericardium also takes part in the inflammation. Gendrin has assumed a special form, fibro-pericarditis, but this term expresses a limita- tion of the inflammation to this layer of tissue, such as scarcely ever exists. Even the mediastinal connective tissue may be in- volved in the process, leading to the development of indurated bands and tough adhesions. w In rare cases of purulent pericar- ditis we find little collections of pus in the fibrous layer of the pericardium. Not uncommonly, but by no means constantly, we find signs of inflammation upon the pleura pericardii, whereby agglutina- tions and adhesions may occur with the adjacent portions of the A case of the sort is contributed by Th. Salter. See Virchow, op. cit. 570 BAUER.—DISEASES OF THE PERICARDIUM. lungs, or with the costal pleura, if the lungs have previously been pushed aside. The remaining visceral lesions, which may occur simulta- neously with inflammations of the pericardium, belong partly to the primary diseases, and are in part referable to the same causes which produced the pericarditis. Only a few consecutive phe- nomena find their explanation in pericarditis, and they are pre- cisely the symptoms and results of the stasis which is very likely to occur from a high degree of concomitant affection of the mus- cular substance of the heart. Pathology. General Picture of the Disease. If, as happens in the great majority of cases, the pericarditis comes on secondarily in the course of an acute or chronic disease, the phenomena of the fundamental affection are, as a rule, not essentially, or at least not suddenly, modified. Moreover, on an analysis of cases of idiopathic pericarditis, those phenomena which can be ascertained without physical examination are not sufficiently definite and constant to form the ground of a posi- tive diagnosis. The subjective symptoms which occur in acute diffuse peri- carditis are not usually of much significance,1 consisting for the most part of a pressure-like pain or a dull sense of oppression in the precordial region. Commonly, also, there is tenderness of the epigastrium, particularly on external pressure. Some- times patients complain of difficulty of breathing and of palpi- tation. In idiopathic cases, or in those occurring in the course of chronic disease, the general condition may suffer but slight disturbance, especially in impassive persons, so that patients of this sort continue to go about. Sooner or later, as a rule, a feeling of languor and indisposition to bodily exertion sets in 1 It is probable that idiosyncrasy has an influence in this matter. Thus Baeumler has published cases in which there was the peculiarity of a tolerably characteristic assem- blage of symptoms. Possibly such cases may be more often met with amongst the well- to-do classes, in private practice, than in hospital patients. PERICARDITIS.—PATHOLOGY. 571 All these phenomena may be wanting, or, on the other hand, the picture may be one in which the wildest disturbances figure, whilst extreme dyspnoea, orthopncea, and sleeplessness, fainting- fits, etc., justify the portrayal which the older physicians made of pericarditis. Under such circumstances, the phenomena essentially resemble those caused by a myocarditis or muscular degeneration, or a valvular affection without compensation. The course of the fever in pericarditis is not at all character- istic ; as a rule, the elevation of temperature is slight, and, if fever existed already before the outbreak of the pericarditis, the newly developed inflammation does not always exert a percep- tible influence upon the febrile temperature. The only sure signs of pericarditis, whether secondary or idiopathic, are the physical changes. Not only do these render the diagnosis possible, but they also give information as to the course of the disease, at least as regards the exudation. On account of fibrinous deposits upon the layers of the pericardium, friction sounds are produced by the rubbing of these upon each other. These sounds may decrease or disappear upon the occur- rence of a larger amount of exudation into the pericardium, and so, too, agglutinations and adhesions may cause them to cease. If the fluid in the pericardium becomes diminished, the friction sound thereupon reappears or becomes increased in intensity, to disappear finally after a varying length of time. In proportion as the fluid distends the pericardium, the cardiac dulness of the anterior thoracic wall increases in inten- sity and area, and at the same time, in the majority of cases, the area of dulness shows a characteristic form, whereby we are enabled to recognize enlarged pericardial dulness as such. The shape is that of a truncated triangle, with the apex turned up- wards and the base downwards. When the effusion is absorbed, the dulness diminishes again, and may return to a perfectly normal extent. The behavior of the apex-beat furnishes very valuable infor- mation. At first, and for some time, it may be normal or even increased in force, but, in proportion as the fluid exudation forces the heart's apex away from the chest wall, it becomes weaker, and is at last wholly extinguished. 572 BAUER.—DISEASES OF THE PERICARDIUM. Very abundant exudations may visibly alter the shape of the thorax, compress the lungs, and, by pressure upon the neighboring organs, effect a change in their position. The pressure of the fluid upon the heart and the great vascular trunks may interfere with the circulation in variable degree. Other symptoms of pressure and compression occasionally occur on the part of the distended pericardium, although more rarely. The occurrence of exudation in the pericardium, the existence of a friction-sound, and increase of the cardiac dulness constitute the essential features of every case of pericarditis, which always repeat themselves. But, so soon as we go a step further, we come upon a great multiplicity in the objective symptoms also. We must seek for definite causes of this variability, and here it appears that the quantity and character of the exudation, the condition of the cardiac muscle, and the character of the fun- damental disease have a most important influence upon the remaining complex of symptoms of pericarditis. It is of signifi- cance, furthermore, whether the affection arises and follows its course acutely or chronically. Very commonly, too, other dis- eases coexist with the inflammation of the pericardium, and if these chance to involve impediments to the circulation and to respiration—as is the case, for example, with a pneumonia or a pleurisy—a much severer assemblage of symptoms will, as a matter of course, result from this combination than from a pericarditis alone. In conformity with the variability of the symptoms, the importance and gravity of the disease are also various. In order to a thorough elucidation of this multiplicity of the phenomena and of the causes thereof, some authors, such as W. Stokes, have attempted to make a sort of division of pericarditis, accord- ing to the severity of the symptoms. Of course, there are no strict grounds or rules for such a distinction, which, however, tends to facilitate a general survey of the rather complicated conditions. Stokes has distinguished three grades of intensity in peri- carditis, using as distinctive marks the amount of fluid effusion on the one hand, and on the other hand the implication of the muscular structure. In accordance with this plan, we may refer PERICARDITIS. —PATHOLOGY. 573 to a first group all those numerous cases which remain circum- scribed, as well as all those which, while indeed they affect the whole pericardium, run their course without a great effusion of fluid and without involving the muscular substance in an acute manner. Although under this arrangement pericarditis does not figure as the final phe- nomenon of a fatal fundamental disease, and may perhaps even give rise to a purulent exudation; and although it may occur under circumstances in which a slight additional functional disturbance may prove unbearable, we may yet characterize as benign those cases which, as a rule, occasion no very serious illness. Even in the presence of manifold complications a pericarditis of this sort gives rise to no great increase of the disturbances and dangers, and may proceed to a favorable result. Spontaneous pericarditis may behave thus. It is very common to see inflammation of the pericardium behave thus in rheumatic polyarthritis, as well as in pleurisy and pneumonia, valvular lesions, etc. Baeumler' has recently called attention to the short duration of many cases of idiopathic pericarditis, especially when circumscribed, so that so transitory an illness may well remain unobserved, and we cannot wonder if the traces of recent peri- carditis are found at autopsies, where during life this disease had been entirely overlooked. Baeumler had an opportunity of making thorough observations on himself. In another example of the sort the whole process lasted four days, but the symptoms were very well marked; slight fever was present. The patient became suddenly ill, with pain in the epigastrium, which was increased by each inspiration and by any movement, particularly forwards; the aspect was that of a severe affection, but for a short time only. At the first examination nothing was found but tenderness of the epigastrium on pressure; somewhat later a circum- scribed friction-sound appeared, which disappeared after twenty-four hours, with- out any change having occurred in the cardiac dulness. Besides the pain in the epigastrium, there were similar pains in the region of the left shoulder, radiating thence towards the left ear and the left arm. At the end of four days, perfect health, both objective and subjective, was regained. So well-defiued an assemblage of symptoms, especially of the subjective ones, seems chiefly to be peculiar only on account of the acute idiopathic pericarditis, whilst secondary cases, analogous in other respects, may appear with very trifling symptoms. The following case from v. Ziemssen's Clinic is an example of the sort: Mitral stenosis, croupous pneumonia, fibrous pericarditis, endocarditis with aortic insufficiency. K. A., a butcher's wife, forty-seven years old, had been brought to the clinic in the year 1874, with rheumatic polyarthritis, was treated with plaster- of-Paris bandages, and in the course of that affection had acquired the valvular disease first mentioned. On February 16, 1876, she fell ill with a smart chill, fol- 1 Transact, of the Clinical Soc. V. 1872. 574 BAUER.—DISEASES OF THE PERICARDIUM. lowed the next day by pain in the left side, shortness of breath, cough, and bloody expectoration. On February 22. a pleuropneumonia was found, with hepatization of the left lower lobe, the progress of which was shown by the fact that up to March 15, long after the fall of temperature, fresh sputa highly tinged with blood were ejected. Resolution took place very slowly, a loud pleuritic friction sound was to be heard for a long time over the left lateral region. On March 5th a rough murmur, following the systole, appeared over the origin of the aorta, whilst up to that time only the presystolic murmurs at the apex, with a faint whirring, and marked accen- tuation of the second pulmonic sound, had been present, with the sounds otherwise normal. The pericarditis produced no recognizable fluid exudation, the apex-beat and area of dulness remained unchanged, although the friction-sound became diffused during the following days, occurring with two intermissions. The acces- sion of the pericarditis was not announced by any new subjective symptom; the frequency and character of the pulse, from sixty to seventy-six beats, as well as the temperature remained unaltered. Moreover, the occurrence, on March 7, of a new soft diastolic murmur, of a humming character, along the course of the aorta, pro- duced no change. On March 14 the pericardial friction had entirely disappeared; the new diastolic aortic murmur remained constant. The patient left the institution in good condition. Day of Dis. Fig. 1. F. 105.8° 104.° 102.3° 100.4° 98.6° 96.8° iiiiiiiiiii !S"!!!!!!! MHiiinii jiiiiiirmr IllllllllfJII iiiiiiiiiii 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 2G 27 iiiiiiiiiiiiiiiiiiiiiii IMIIIIIIIIIIIIIIIII IfilVi ' illAiiHimimiiiiiiiiiii Feb. 22 IIJIIUKiUIMI IIINIIHIIIII immiiiiiii IMIMiMlMlllB 23 24* 25 26 27 28 29 1 2 3 4 5 6 7 8 9 10 11 12 13 14 * Two drachms of salicylate of soda. Observations, at first, every second hour during the day, then thrice and twice a day, in the axilla. To a second group belong chiefly those cases which are accom- panied with abundant fluid exudation, without the muscular substance undergoing much change. Such cases may be pri- mary or secondary, they may occur with slight or with very severe general phenomena, and the quantity of the exudation may give rise to severe symptoms. In such cases, if no aggravating constitutional conditions be present, if the pa- tient be not advanced in years, and if the fundamental disease involve no unfavorable 99934857 PERICARDITIS. —PATHOLOGY. 575 presumption, the termination is generally a favorable one, either with perfect resti- tutio ad integrum, or with adhesions. However, the amount of the exudation may cause death. At most, only serous or sero-fibrinous exudations are here considered. Hemorrhagic effusions generally derive their unfavorable character from previous constitutional troubles. Purulent exudations seldom prove fatal by their quantity, but in conse- quence of the primary and original change, or by retardation of absorption and by the muscular degeneration which finally results therefrom. The following case, from v. Ziemssen's Clinic, may serve as an example of a pericarditis with large effusion and a favorable result. Rheumatic polyarthritis ; tero-fibrinous pericarditis; endocarditis; double exudative pleurisy ; catarrhal icterus. A man-servant, thirty-five years old, a moderate drinker, previously always healthy, fell ill with acute articular rheumatism, with an initial chill, after having already had subacute inflammation of several joints. On admission, numerous joints were seen to be affected ; no pain in the chest. Apex-beat faintly perceptible iu the normal locality. First sound feeble and indistinct at the apex, and equally so over the pulmonalis, where the second sound was somewhat accentuated. Pulse 104, bounding, rather tense, regular, and out of proportion to the weak heart- sounds. At the upper part of the left side of the chest, in front, below the second rib, the percussion note was less intense and higher in pitch than on the right side, passing abruptly into the area of comparative cardiac dulness. Respiration moderately frequent. Urine free from albumen, with a specific gravity of 1031. On the following day, November 8, abatement of the articular pains, a feeling of pressure and distention in the pit of the stomach, somewhat increased by external pressure. Skin very dry and hot. Pulse very tense, 88 in the morning, 126 in the evening. Apex-beat in the fourth intercostal space, three ctm. externally to the nip- ple-line. Absolute cardiac dulness increased only a little towards the right, and not at all upwards; the relative cardiac dulness begins above at the upper border of the third costal cartilage, and extends towards the right as far as the right side of the Bternum. Heart-sounds indistinct at the apex, accompanied by a soft grating mur- mur ; in the third intercostal space, near the left border of the sternum, a loud, sharp, rasping friction murmur is audible and distinctly perceptible to the touch. Carotid sounds clear. On November 9 the epigastric pressure had entirely disap- peared ; patient had a very restless night, the joint pains being somewhat increased. Apex-beat still present, but feeble; slight increase of the absolute cardiac dulness towards the right as far as the middle of the sternum ; over the mitral, a systolic blowing murmur ; over almost the whole heart, a loud, harsh friction-sound, in two intermissions with the systole and diastole, but no longer to be felt. The relative cardiac dulness extends to the lower border of the second costal cartilage, reaches to the left about four ctm. beyond the site of the apex-beat, and to the right somewhat beyond the sternal line. Pulse 104 in the morning, 144 in the evening, regular, very tense. November 10.—Articular pains less severe again. Murmurs unchanged, to be felt slightly again on firm pressure in the third intercostal space. No pain in the 576 BAUER.—DISEASES OF THE PERICARDIUM. chest or epigastrium. Pleuritic effusion on the left side. Pulse, 88 in the morning, 104 in the evening, regular, full, and tense; respirations 36. No further change in the absolute cardiac dulness, the base of which measures 11 ctm., the right side 8 ctm., the diagonal, from the summit to the site of the apex-beat, which is still feebly perceptible, 11 ctm. The relative cardiac dulness has still further extended, and surrounds the absolute dulness with a belt of about two finger-breadths, which is materially increased when the patient sits upright. November 11.—Double pleuritic effusion; additional joints affected; apex-beat felt feebly in the fourth intercostal space, somewhat within the nipple-line. Absolute and relative cardiac dulness perceptibly smaller; second pulmonic sound moderately accentuated; heart-sounds more easily distinguished than hitherto; a loud friction-sound at the left border of the sternum. Moderate general icterus, liver not enlarged and not tender. Pulse, 120 in the morning, 144 in the evening, rather jerky. The area of cardiac dulness changes little with the upright position; the friction sound becomes softer. November 12.—Icterus somewhat less; no pain in the chest; joints free, with the exception of a little swelling of the knees. Apex-beat very feebly perceptible in the fourth intercostal space, about 2 ctm. inside the nipple-line. The friction- sound at the left border of the sternum is very soft; a newly-developed friction- murmur is found in the region of the tricuspid. Carotid sounds clear. The cardiac dulness now extends only to the lower border of the third left costal cartilage; skin moist in the morning, dry and hot in the evening; pulse 100 morning and evening, slightly jerky. November 13.—A restless night, with renewed articular pains. Heart-sounds clearer; friction-sound still soft. Pleuritic effusion unchanged. A stitch-like pain on inspiration in the region of the heart. Apex-beat still weak; the relative dulness no longer extends beyond it, but reaches to the right beyond the right border of the sternum. The absolute cardiac dulness is nearly normal. Fig. 2. 6 7 8 9 10 11 12 1.3 14 15 16 17 18 19 20 21 22 Morning and evening temperature (in the axilla). November 14.—Articular pains not much changed. Friction-sound has almost entirely disappeared; a soft murmur lags after the second aortic sound. At the apex of the heart a systolic blowing murmur and an accentuation of the second PERICARDITIS.—PATHOLOGY. 577 pulmonic sound. The relative cardiac dulness is scarcely increased in breadth reaching to the right border of the sternum. The icterus is gone, as well as the pain in the region of the heart. Apex-beat again plainly to be felt in the fourth intercostal space, 2 ctm. to the inside of the nipple-line. Pleuritic effusion still present. From this time on the friction-murmur disappeared; the pericarditis had run its course. The polyarthritis, with the endocarditis and pleurisy, lasted until Novem- ber 20, and left a slight valvular deficiency. . 11 To a third group belong those BSSSSBSSSf' cases in which disease of the cardiac = iSSSSSBBBESSi 5 muscle appears among the symptoms, 5SS3 S333S or constitutes the chief feature. The "bSSBBBSBBBJ phenomena depending thereon may *E SSSS5EBS be present in very various degrees of s Ifi BBSBSB£2Ss!. intensity. To this category belong _|SS SESSSS- also many cases of purulent peri- 5HHBm555hS 5 carditis, as well as all chronic injlam- "E asaH5HH; : motions of the pericardium, almost -IbSs^S—5S S5| - without exception. " BBBB—iSSBBBBu '■■■■ BHIi^iaHM \m 55m«2BJ Paralysis of the heart may occur in an acute ^[BBBBSSHSBBl- § way in consequence of acute myocarditis, and ™ H SELslSaMmHM | under such circumstances death may take place fa ^ SB BBSBBBS| speedily and quite suddenly ; or a degeneration <* ■ BS^ SB - of the substance of the heart may develop grad- X|B nSSSS BL a ually, generally by layers; the impelling power BSft^BBBBS » constantly diminishes, stases occur, general '"B igJS ■—g° | dropsy, and finally death. We then find the -B SSSSSSSSSL I heart more or less degenerated, atrophied, or, if BBBE^SBBBBB the fluid effusion have been absorbed in the |SSSSSS*i2B E meantime, the cavities dilated. S5SSS39SSSS& The acute, as well as the more chronic ■■ mSssiiwmwmwmSBm changes, may remain stationary, ending in by- r,„ iSBBBBBBBSS pertrophy preceded by dilatation. J BBS^"™ SESSS Idiopathic pericarditis, with hemorrhagic % ^ ISSSinSEBSSS exudation and muscular degeneration; death.— © IBBBSSiiSSSS A man fifty-two years old, always before healthy, ° ~ |BBE5SSiBBBBB| was living under favorable conditions. He P '«._ fe %. h S> K dated his ill-health five weeks back, when he S I ° ^ $ fell ill with stitch-like pains in the chest, could no longer lie on the left side, and suffered much from cough, without expectoration. The pains in the side lasted only VOL. VI.—37 500746267�0 �5026848763�57 578 BAUER.—DISEASES OF THE PERICARDIUM. two days, and then the appetite and strength gradually failed. Bowels irregular; sleep good; occasional dyspnoea; powerfully built and well nourished, apparently a drinker. Radial artery very small; pulse uncommonly faint, and rendered more so on inspiration, without wholly disappearing; 104, regular. Moderate emphysema. The apex of the right lung lies somewhat deeper than the left, and is less resonant on percussion. Expiratory sound somewhat prolonged. The cardiac area is enormously enlarged laterally and upwards, of a triangular shape; apex-beat nowhere perceptible, but intestinal resonance immediately below the sixth rib. On standing, the cardiac area becomes strikingly enlarged, especially towards the right—about 3 ctm. On lying down, the base measures 19 ctm., the right side 16 ctm., the left side 17 ctm.; from the apex to the base 13 ctm. A soft, scraping friction-sound is heard over the sternum; heart sounds clear, but very feeble; hepatic dulness somewhat diminished in breadth, and the left lobe appears small. Spleen 13x8 ctm. Slight distention and undulation in the veins of the neck. Considera- ble cough, with frothy, mucous sputum. Scrotum large and lax, without cheesy deposits. Urine of a dusky brown, without sediment or albumen; 400 cc.; specific gravity 1021. No dropsy. During the progress of the case the area of cardiac dulness became perceptibly smaller, but the outline was somewhat irregular, and the inspiratory movement of the border of the lung was very slight. But the condition of the pulse became still worse. It disappeared entirely on inspiration. Extreme cyanosis was developed, and dropsy, ending in death. At the autopsy the pericardium was found enormously distended by an effusion of a faintly bloody tinge. The borders of the lungs were moderately distended and adherent to the pericardium. In both lungs there were scattered cirrhotic nodules. Pericardium thickened, with villous, tufted deposits on the inner surface of both the visceral and the parietal layers, single fibrinous bands passing from one layer to the other. The heart is enlarged, cuts easily, and shows quite a layer of fat beneath the exudation; muscular substance pale and very fragile; valves healthy; liver somewhat diminished in size, of a nutmeg color. Kidneys rather small; granular and scarred on the surface, (v. Ziemssen's Clinic.) Hemorrhagic pericarditis is met with under various con- ditions, and does not always give rise to a peculiar train of symptoms. Signs of anaemia and its consequences occur only when there is an abundant effusion of blood into the pericardial sac. This is preeminently the case in pericarditis due to scurvy, as we learn from the accounts of it as occurring in the northern maritime portions of Russia. Together with the symptoms of an acute exudative pericarditis, marked prostration suddenly occurs, accelerated respiration, with great anxiety, swelling of the jugular veins, imperceptible pulse, cyanosis, coldness of promi- PERICARDITIS.—PATHOLOGY. 579 nent parts, and dilatation of the pupils. Consciousness remains unimpaired until death, which generally occurs suddenly. In chronic cases of scorbutic pericarditis the cardiac affection is preceded by so-called rheumatic fever symptoms. The effusion takes place more gradually, and accordingly the phenomena of collapse appear with less severity and suddenness, and the danger to life is not so immediate.1 A special interest attaches to the chronic inflammations of the pericardium, whether they assume the chronic character, by repeated extensions of inflammation following an acute beginning, or whether they creep on insidiously, without local symptoms and often also without fever, attention not being directed to an examination of the heart until difficulty of breathing, changes in the pulse, etc., supervene. In such cases the effusion is commonly hemorrhagic, and the duration of the illness often extends over many weeks or months. The result is generally fatal by second- ary degeneration of the heart and atrophy, and indeed in favor- able cases obliteration of the pericardial sac, dilatation of the ventricles, etc., always occur. The following case from v. Ziemssen's Clinic affords a very striking example: Chronic pericarditis, degeneration of the cardiac muscle.—A man, thirty years old, a confirmed drinker, very corpulent, had always been healthy, except for a contused wound which he had received in the Franco-Prussian war, until Easter of 1874, when he first fell ill with rheumatic pains, and then with a croupous pneumonia of the left side, which ran its course with marked adynamic symptoms and with a great amount of dilatation of the right ventricle. After this he again felt perfectly well and strong until the end of May, when he was taken ill, first with gastric symptoms, then with stitch-like pains in the chest, dyspnoea, and oppression at the epigastrium. Moderate oedema, face somewhat bloated, complexion yellowish and bluish. Abdo- men swollen with ascites. Subjective and objective dyspnoea, respiration forty. Pulse tremulous, scarcely perceptible in the radial, whilst in the carotid it was so irregular that its frequency could not be determined. Right external jugular vein tense and swollen, not pulsating; the same, less marked, on the left side. Liver markedly swollen, without pulsation. No apex-beat in the region of the heart, nothing more than a diffused tremor being observable between the acts of respira- tion. The cardiac dulness reaches from the right parasternal line to the line of the anterior boundary of the left axilla, and upwards to the jugular fossa, forming a 1 Kybei's article, Med. Zeitg. Russl. 1847. I have not been able to get access to it in the original; so I have taken these statements from Friedreich., loc. cit. 580 BAUER.—DISEASES OF THE PERICARDIUM. triangle truncated superiorly. The breadth of the area, at the level of the nipple, measures twenty-five ctm.; the height, at the left border of the sternum, eighteen ctm. The area is somewhat larger still in the standing position. Heart sounds clear everywhere, but very weak and distant. The upper lobe of the left lung is very much compressed, that of the lower lobe less so. A moderate amount of free movable fluid is found in the right side of the thorax. His sleep is restless and interrupted ; occasional orthopnoea. The appetite is poor; bowels irregular, some- times diarrhcea. Temperature elevated, but not constant. Fig. 4 Daily quantities of urine during the first part of the disease, May 20th to September 4th. His condition improved constantly, although with many fluctuations. The pericardial effusion was partially absorbed, a friction sound occurred, and the dulness diminished in extent; the state of the pulse improved, and the dropsy disappeared entirely, so that the patient left the institution after the lapse of four months. The variations in the amount of water excreted by the kidneys are of Fig. 5. Daily quantities of urine during the second part of the disease, December 14 to April 19. interest, since the means which served to strengthen the blood-pressure caused a decided increase in the quantity of urine. The patient left the institution at the beginning of October, and returned December 14, in a very sad condition. Without any essential change in the state of the heart, the area of cardiac dulness had constantly enlarged, and the outlines had become somewhat irregular. The phenomena of obstructed circulation and the cardiac weakness constantly increased, the dropsy was very considerable, and the patient died April 19. Autopsy.—Cyanotic colorations ; very great dropsy ; a great deal of serous fluid in the pleural cavities and in the abdomen. The anterior borders of the lungs were still adherent in many places. The whole pericardium was thickened and indu- 2 PERICARDITIS.—PHYSICAL SIGXS. 581 rated; its cavity contained a moderate amount of hemorrhagic effusion, and its serous surfaces were covered with fine tufts. The apex of the heart, together with both auricles, was drawn backwards by a band as thick as the finger. The visceral layer of the pericardium was also thickened, the muscle thinned, the cavities nar- rowed, and all the valves normal. The fibrillte of the cardiac muscle were found to have undergone thorough fatty degeneration; the bundles were strewn with laro-e oil globules. There was also a slight degree of connective-tissue new formation and hyaline degeneration. For the rest, there were only the signs of long-standing stasis. We must still mention briefly the pericarditis of children. According to the statements of Rilliet and Barthez, this disease is extraordinarily rare in children under six years of age, but it has been known to occur in the earliest periods of life, and even during the fcetal state. In childhood, too, most cases are of a secondary nature. Kerchensteiner has published a case of idiopathic pericarditis in a girl eleven months old. Circumscribed pericarditis in children remains latent, as a rule. Even the diffuse variety shows no characteristic phe- nomena, since the pain is absent or not to be discovered; and the objective signs are commonly very ill marked—the effusion being often very scanty, not more than a few tea-spoonfuls. In other instances, however, the amount of effusion is very con- siderable. Large effusions appear to affect the functional activity of the heart more rapidly in children than in adults, and to occasion the earlier occurrence of signs of disturbance of the circulation, even although, as in idiopathic cases, there are no complications present. Chronic pericarditis also occurs in children. In early infancy diffuse pericarditis is certainly a very dan- gerous disease, generally leading to speedy death. In later childhood its course and result are subject to the same influences as in adults. Physical Signs. Inspection.—In rather moderate effusions into the pericardial sac, the thorax may, as a result, suffer a visible alteration of form, provided the chest wall be sufficiently yielding, as is par- ticularly the case in young persons and in the female sex. On 582 BAUER.—DISEASES OF THE PERICARDIUM. the other hand, an unyielding state of the thorax, shrinking of the lung, and extensive pleuritic adhesions tend to prevent a perceptible change of configuration. With these provisos, the region of the heart becomes some- what more bulging and prominent, in consequence of an abun- dant pericardial effusion, and the left nipple may be situated somewhat higher than the right one. We often see, too, an increased distention of the corresponding intercostal spaces and a diminished respiratory movement of the same. We should not forget, however, that, even in considerable enlargements of the heart itself, an increased prominence of the cardiac region may also take place. According to Duchek, in pericardial effusions we have a uniform dilatation of the left half of the thorax, the same as in pleuritic effusions; while, in consequence of the increased pressure in the left side of the chest, the ribs remain in the inspira- tory position. Duchek is in accord with Corvisart, Philipp, and Gendrin, whilst j nearly all the more recent authors speak only of an increased prominence of the I region of the heart. Inasmuch as the pressure in the left side of the chest is actu- ally increased by a large pericardial effusion, we must agree with Duchek to this extent, that the left side of the thorax may undergo a certain degree of enlarge- ment from this cause. But the enlargement is not uniform, as in pleuritic effusion, but the particular region of the heart is the most bulged out, because the pressure of the pericardium filled with fluid cannot be exerted equally in all directions, but manifestly must be directed chiefly from behind forwards. The costal cartilages are thus arched forwards, and at the same time the ribs raised in toto. By this feature the dilatation of the thorax from pleuritic effusion is distinguished from that of pericardial effusion. In the opinion of some observers, such as Gendrin, the enlargement referred to is partly due to inflammatory paralysis of the intercostal muscles. Although this theory is somewhat fanciful, I have yet seen in many patients with pericarditis excessive tenderness of the intercostal spaces without concomitant pleurisy, and we must thence infer that in these cases the intercostal muscles participate in the inflam- mation. In excessive pericardial effusions the epigastrium is also sometimes seen to be highly swollen, as was first observed by Auenbrugger. This phenomenon is partly due to a forcing down- wards of the diaphragm and displacement of the liver, and partly to swelling of this organ on account of stasis. It has been stated, too, that the skin of the prsecordial region PERICARDITIS.—PHYSICAL SIGNS 583 occasionally shows an cedematous condition in pericardial effu- sions. In regard to this, Bamberger remarks that he has seen such an oedema only in connection with accompanying general dropsy ; and such, indeed, will always be the case. An undulating motion, visible in several intercostal spaces, has been described by many authors, and first by Senac, and referred to the fluid being set in undula- tory motion by the movements of the heart. This view arises from confounding such motion with visible contractions of the heart itself. On the contrary, a visible undulation of this sort upon the thorax tends to show the non-existence of a large pericardial effusion (Cejka). Under some circumstances palpation gives evidence of im- portant changes. This is especially true of a careful examina- tion of the apex-beat. If the fibrinous element preponderate in the exudation, any alterations of the apex-beat which may be present possess nothing characteristic, and serve only to confirm such abnormalities as are partly recognized by the pulse, such as irregularity, acceleration, and strengthening of the heart's action ; in the latter case the apex-beat may also be strengthened and somewhat diffused. The pericardium is distended by the fluid effusion, and the heart thus becomes endowed with greater mobility than it possesses under normal conditions. Accordingly, we are some- times enabled to make out a greater capacity for change of position on the part of the apex-beat in conformity with changes in the patient's position than was the case before. It was formerly considered a sign of pericardial effusion if, on changing the patient's position, an alteration took place in the site of the apex-beat, apart from the degree of mobility of the apex. But a variation in the locality of the apex-beat is common likewise in health; and, according to numerous observations by Gerhardt, in very many healthy persons, upon lying on the left side, the apex-beat moves about 2 ctm. further towards the left. As we have already mentioned, the cavity of the pericardium is not entirely filled by the heart, so that a certain mobility of the latter is allowed on change of posture. In regard to the degree of this mobility, pretty wide individual differ- ences prevail. Apart from a readier mobility of the apex-beat on change of the patient's posture—as a sign of increased mobility of the heart—its position is rather frequently changed in such a manner 584 BAUER.—DISEASES OF THE PERICARDIUM. that it is pushed' somewhat further outwards (to the left), and occasionally also a little lower down. Inasmuch as the effusion into the pericardium first collects about the base, the latter is turned downwards, the heart lies rather more horizontal, and therefore the apex must turn outwards. It is only when the diaphragm is pressed down by the effusion that the heart's apex descends. In proportion as the fluid fills the whole pericardial sac and surrounds the heart on all sides, the apex-beat grows weaker, and may finally wholly disappear, because the fluid presses the apex away from the chest-wall, and thus prevents the beating of the apex against it. Occasionally, indeed, according to Ham- mernik, a slight sinking in occurs with the systole in place of the previous bulging. The weaker the apex-beat was at the commencement, the earlier, of course, will it disappear, since the energy of the heart's action diminishes with the progress of the exudation. Vice versa, a much thicker layer of exudation will be required to produce a disappearance of the apex-beat in case the heart's action is very powerful, and especially if hypertrophy be already present. If, in consequence of old (circumscribed) adhesions, or also as the mere result of agglutinations between the cardiac and the parietal layers, the crowding down of the heart's apex away from the anterior thoracic wall has been ren- dered impossible by the imprisoned fluid, the apex-beat may continue to be perceptible. Under any circumstances, the disappearance of the apex-beat is an important symptom, all the more valuable if a dispropor- tionately full and tense pulse show that it cannot be owing to weakened power of the heart. We not unfrequently observe that the apex-beat, which the effusion had caused to disappear in the dorsal decubitus, becomes apparent again on bending the body forwards in the sitting or standing posture, because the heart falls further forwards and forces the fluid back. The friction of rough pericardial surfaces is but compara- tively seldom to be felt, as it requires a striking intensity of the friction sound ; in such cases we feel, with the flat hand or with the fingers singly, a more or less diffused, multiple PERICARDITIS.—PHYSICAL SIGXS. 585 and strong scratching, shoving, or creaking. It is not generally difficult for a skilled observer to distinguish a rubbing from a purring. In many cases it is possible to intensify the percepti- ble rubbing sensation by pressure on separate intercostal spaces, or to first render it perceptible in this way. A feeling of fluctuation in those intercostal spaces against which the pericar- dium, filled with fluid, lies, is indeed mentioned by some, but is denied by author- itative observers, such as Bamberger. A priori, it is, in truth, very unlikely that under the conditions existing a fluctuation should be perceptible. Moreover, Friedreich justly rejects Zehetmayer's statement, that with his out- spread hand he had obtained a sensation as if the heart were beating in several places at once, so that it was impossible to distinguish at what point the true apex- beat took place, and where he felt a movement communicated to the fluid. Percussion.—The cardiac dulness can undergo no change until a certain amount of fluid has been effused into the cavity of the pericardium. The pericardium becomes distended by the exudation, and as a consequence the cardiac dulness is extended and increased, and its figure, as mapped out on the anterior thoracic wall, shows, in the majority of cases, a characteristic form. How great a quantity of fluid is necessary, to be recog- nizable by percussion, can be only approximatively stated ; as a general thing, we must not expect notable changes of the cardiac dulness if the quantity be less than 100 cubic centimetres. But many circumstances may conspire to render this approximative measurement worthless. As a rule, pericardial effusion enlarges the area of relative as well as that of absolute cardiac dulness. Observers are still at variance as to whether it is more correct to lay the greater stress in diagnosis upon the extent of perfect lack of resonance or upon that of diminished resonance—/. e., upon absolute or rela- tive cardiac dulness. Bearing in mind the various statements in literature seeming to show the absence of any change in the car- diac dulness in a considerable number of cases, which statements refer altogether to the absolute cardiac dulness, and taking coun- sel of our own experience, we shall reach the conclusion, that a knowledge of the relative cardiac dulness is of the greater value in the diagnosis of pericardial effusions, since indeed the absolute 586 BAUER.—DISEASES OF THE PERICARDIUM. cardiac dulness not uncommonly, in cases of well-marked effu- sion, shows little or no alteration. The increased intensity of the relative dulness is very note- worthy, and by its aid we are the more easily enabled to mark out with perfect clearness and thoroughness the limits of the dulness. The enlargement of the area of relative dulness is due to the fact that the distended pericardium compresses the lungs forward to a greater or less degree. The absolute cardiac dulness enlarges almost in exact proportion as the borders of the lungs are pressed backwards entirely away from the anterior chest wall by the distended pericardium, which does not always take place, and never uniformly. It occurs especially when the pleura pericardii (lamina mediastinalis) is agglutinated to the pleura costalis; therefore all statements which assert the importance of such agglutination in the diagnosis of pericarditis are of value only in so far as they refer to enlargement of the area of absolute cardiac dulness. Besides the quantity of exudation in the pericardium, the intensity and extent of the dulness really depend upon some other factors. Foremost among these is the degree of elasticity of the lungs, since the stiffer and more inelastic is their tissue, the greater resistance do they offer to compression. Such lungs, particularly if emphysematous, are not so easily forced away from the chest wall and compressed, and, moreover, they are more voluminous, and less of the pericardium comes in contact with the anterior wall of the chest. If the borders of the lungs be firmly adherent they cannot retreat, but can only be com- pressed. Partial adhesions of this sort may cause the dulness to assume an irregular outline ; this happens to a still greater extent in consequence of old partial adhesions of the pericardial layers to each other, since in that case the distention of the pericardium takes place in whatever direction is rendered pos- sible by the particular sort of adhesion. It is the different degrees of elasticity of the lung tissue which, above all else, determines the individual varieties of the state of the absolute and relative cardiac dulness in exudations of like amount. Hammemik sought to explain these differ- ences by assuming a superficial (normal) and a deep position of the pericardium. PERICARDITIS.—PHYSICAL SIGNS. 587 It is true that in certain persons we find the heart more or less movable, more or less covered with lung, but the folding of the pericardium upon the anterior chest wall and its fixation there by pulmonary tension, assumed by Hammernik, do not exist. According to him, on lying down, and as the result of exudations, the pericardium is raised from its firm position and at the same time displaced. The bulk and the degree of elasticity of the lungs are sufficient to produce the differences which have been mentioned in the dulness in pericardial effusions. The increased intensity and area of the cardiac dulness are all the more significant when suddenly developed under the eye of the observer. If the change occurs slowly, it will certainly be very difficult on some occasions to distinguish small effusions, without a friction-sound, from actual or apparent enlargement of the heart. It is only in rare cases that large effusions present difficulties, on account of the extent as well as the form of the dulness. The enlarged and more intense cardiac dulness of pericardial effusions may be confounded with enlargement of the heart's volume, as well as with denudation of the organ or retraction, fixation, and diminished size of the lungs, allowing a larger portion of the anterior surface of the heart to come into contact with the chest wall. Error may arise, too, from thickening of the anterior border of one or both lungs, from sacculated pleuritic effusion, from tumors and neoplasms. By calling all the facts to our aid, a sure diagnosis is possible, as a rule. The enlargement of the area of relative cardiac dulness takes place in the direction of the heart's length as well as in that of its breadth, and it not uncommonly happens that, together with the other signs of pericarditis, a suddenly developed increase in the breadth of the cardiac dulness, to the extent of one or two ringer-breadths, may suffice to show the probability of a trifling effusion. As a rule, however, the increase in the direction of the long axis preponderates. In larger effusions it may happen that the apex-beat is still to be felt, and that the left boundary-line of the area of relative dulness extends towards the left a considerable distance beyond the site of the apex-beat, because the pericardium is lifted away from the heart by the fluid (Traube, Gerhardt). This is the only condition under which the cardiac dulness can extend beyond the situation of the apex-beat towards the left, and therefore the presence of this symptom is a sure sign of pericardial effusion. 588 BAUER.—DISEASES OF THE PERICARDIUM. The outline of the enlarged pericardial dulness upon the an- terior thoracic wall constitutes in the majority of cases a triangle, the apex of which is directed upwards and its base downwards. Von Stoffela (Oppolzer's Lectures) believes that at the beginning of the effusion the dulness forms a similar triangle with the base directed upwards, and that this is reversed only with the increase of the fluid. This view does not accord with obser- vation, and rests upon the erroneous conception, that at first the effusion accumu- lates at the base of the heart, and distends the pericardium in its breadth; whereas this takes place rather lengthwise, the base of the heart sinking down lower at the same time. The triangular shape of the cardiac dulness is owing to the fluid collecting at first around the base of the heart, and thus distending the pericardium in an upward direction, while the base of the heart sinks as far downwards as its attachments will allow. Now, with a further increase of the effusion, the position of the fluid is governed by the weight and the distensibility of the pericardium, the base of which is independently directed downwards, and thus the form is determined, and not, as Duchek believes, by the separation and recession of the borders of the lungs, since in that case any increase of the heart's volume would necessarily cause a triangular dulness. As a rule, this triangular area of dulness in pericardial effu- sions is considerably enlarged, particularly in its whole upper segment, immediately the patient is brought from the dorsal decubitus to the upright position of the trunk, and to a still greater degree if the body be bent forwards (Gerhardt), since in these postures more of the fluid sinks forwards and impinges upon the chest wall. We find this indeed in enlargement of the heart also,' because a heavy heart sinks forwards, but not in the same degree, and with the same regularity, as in pericardial effu- sions. As regards the size of the triangle, it is of course propor- tionate to the amount of fluid effusion in the pericardium, but not in so strict a manner that we can estimate the quantity of 11 have had an opportunity of observing this state of things in a great number of cases at v. Ziemssen's Clinic, and the same statement may be found in Niemeyer and Seitz. PERICARDITIS.—PHYSICAL SIGNS. 589 the fluid from the size of the area. The reasons for this include nothing more than has been said in regard to the varying degrees of elasticity of the lungs. In effusions of moderate amount, the apex of the triangle usually reaches to the third or second costal cartilage of the left side; but in very large effusions the sternum may be dull on per- cussion throughout its whole extent. The left border of the triangle, in effusions of slight amount, usually runs above the left nipple, or somewhat towards the left from it downwards and outwards. In copious effusions the left border of the triangle may even cut the anterior axillary line, so that the dulness may extend into the axilla itself. The right leg of the triangle is, as a rule, more nearly vertical and less divergent than the left, following the course of the border of the right lung, and reaches to the right border of the sternum, or only a little further to the right. In very large effusions, how- ever, it may even overstep the right mammillary line, so that a large portion of the anterior half of the thorax is taken up by the outline of the heart. The lower limit of the dulness, corresponding to the base of the triangle, is commonly found at the level of the sixth and seventh ribs. We can only partially determine the lower limit directly by percussion, on account of the contiguous left lobe of the liver ; we therefore project the line, from that portion which we have ascertained, towards the right side of the thorax to the point where the hepatic and cardiac areas of dulness come together at an obtuse angle. More rarely still is the diaphragm pushed down on the left side by pericardial effusions—as a rule, only in those of unusual amount or very long standing, so that the dulness reaches down to the eighth rib, and an evident displacement of the left lobe of the liver coexists. As a result of this mobility of the effusion, in obedience to gravitation, we also observe a manifest capacity in the dulness to change its position laterally, so that, for instance, in lying on the right side the dulness extends further to the right. At Lind- wurm's Clinic I saw a young girl with polyarthritis and peri- carditis, in whom, when lying on the right side, the fluid sank so 590 BAUER.—DISEASES OF THE PERICARDIUM. far over to the right that the outline of dulness reached nearly 4 ctm. further to the right than when she was lying on her back. This phenomenon, too, is seen in great enlargement of the heart, but not generally to a very striking extent. On percussing the left subclavicular region, in large pericardial effusions, we find that the pulmonary resonance differs consider- ably, as a rule, from that of the right side ; it is higher in pitch and duller or more or less decidedly tympanitic, in consequence of the compression sustained by those portions of lung which rest upon the pericardium. Graves observed also in one case a hernia- like projection of the apex of the left lung above the* clavicle. Behind, also, it is not rare to find the lower portions of the lungs deficient in air, on account of compression, and they may even be perfectly destitute of air, although very rarely, it is true. Usually there is no difficulty in distinguishing a compression of this kind from a coexisting pleuritic effusion, the presence of the latter being shown by the greater intensity of the dulness, by the linear course of the dulness descending from behind forwards, and by the diminished vocal fremitus, which is generally increased in cases of compression of the lung. In accordance with the importance formerly ascribed to the adhesion of the pleura pericardii to the anterior wall of the chest, the immobility of the borders of the lung during respiration came to be regarded as an important diagnostic sign of pericarditis. This sign is, however, not unfrequently absent in pericarditis ; in fact it is found, as a rule, only in chronic inflammations with extensive adhesions of the borders of the lung, resulting from adhesive pleuritis and other causes. For the diagnosis, therefore, of pericarditis the symptom has no special value. The adhesion of the pericardial pleura to the anterior chest wall, even when the lesion is admittedly extensive, is obviously incapable of rendering the borders of the lung entirely immovable. Of course the adhe- sions act as a restraint upon the excursions of the pulmonary borders, but the resistance is overcome in part by the act of respiration, which forces these portions of the lung against the adherent pleura. This supposed fixation of the borders of the lung from pericarditis is regarded by Traube as of less significance than the presence of a vesicular murmur surrounding the line of PERICARDITIS.—PHYSICAL SIGNS. 591 dulness, indicating that the lung is capable of expansion, not- withstanding some compression and retraction. In proportion as the fluid exudation becomes absorbed, the areas of absolute and relative cardiac dulness in the majority of cases return to their normal limits, often very rapidly. If the adhesions referred to were as common and as important as has been supposed, the absolute cardiac dulness would necessarily remain enlarged in a considerable proportion of cases. The most constant and most trustworthy physical sign of peri- carditis is the pericardial friction sound. This is produced by the roughening of the smooth surface of the serosa by the deposits of fibrin, usually upon both surfaces, but friction may occur even when only one is roughened. Roughness and a resulting friction sound may be occasioned also by concretions, neoplasms, etc., as well as by inflammatory deposits. Collin and Walsh have expressed the opinion that a friction murmur might be excited by dryness of the serous surfaces. This view has been confirmed by the observation of Pleischl, that the marked viscosity of the serous membranes in cholera can give rise to pericardial friction. Moreover, Mettenheimer has heard friction in a case of extravasation into the muscular substance of the heart without pericarditis. These observations have, to be sure, been doubted by many writers, but without good reason. On the other hand, Gendrin is doubtless mistaken in his opinion that friction may occur simply as a result of violent action of the heart. The friction sound usually occurs very early in the disease, continues for several days or weeks, then becomes gradually feebler, and at last disappears ; or it may cease very suddenly from the occurrence of copious effusion or adhesions. The latter may after a while give way, and then the sound reappears. In many cases the occurrence of friction is the first indication of the onset of the disease—in fact, it is generally the only symp- tom ; but it may also be preceded for some time by inflammatory symptoms, such as pain in the cardiac region, fever, etc.1 When considerable pericardial effusion occurs, the friction sound often becomes weaker or disappears entirely; still this is by no means always the case, the friction being sometimes heard and felt where as much as a quart of fluid is present (Cejka). When the 1 See the cases of Mayne, Traube, and others. 592 BAUER.—DISEASES OF THE PERICARDIUM. separated serous surfaces again come in contact with each other, in consequence of absorption of the fluid, the sounds frequently become clear again. It is rare for the friction sound to be absent during the entire course of the disease. This may hap- pen, however, where there is a large effusion poor in fibrin, or where the action of the heart is very feeble, but the cases are exceptional where general adhesions take place so early that the murmur cannot at some time be detected. Frequently the friction sounds are heard first and loudest over the base of the heart, near the origin of the large vessels, and here also the sign may disappear last, because in many cases the deposit of fibrin commences at this point, and here the serous surfaces remain longest in contact when effusion takes place. Still the rule is not invariable ; friction may be heard first and most distinctly over any part of the heart, while over the base it is absent altogether. The friction murmurs differ very much in quality and inten- sity. Sometimes they sound like a slight grazing of rough or viscous surfaces, sometimes like a faint grating, at other times like a loud scraping or creaking, such as is produced by bending new leather or by walking on half-softened snow. Attention was first called to the new-leather murmur (bruit de cuir neuf), as a sign of pericarditis, by Collin. Bouillaud distinguished three varieties of pericar- dial friction sounds: the grazing sound, the new-leather sound, and the grating sound, and he thought that the conditions for the origin of each of these varieties could be accurately determined. Observation, however, teaches that the quality of the friction murmur depends upon other causes than the character of the deposits and false membranes—e. g., on the quantity and position of the serous exudation and the force of the cardiac movements. These are certainly the most common varieties of friction sounds in the pericardium, and their pericardial origin is best determined by these characteristics. But modifications of the most various kinds may occur, which it is impossible to describe clearly or to render intelligible by comparison with familiar sounds. Thus very peculiar combined sounds may be produced by the union of pericardial with endocardial murmurs. In many cases, to be sure, the character of the pericardial friction sound is so striking that its true nature can at once be deter- PERICARDITIS.—PHYSICAL SIGNS. 593 mined with a considerable degree of certainty. In other cases, however, the distinction from endocardial murmurs by this method alone is very difficult or impossible. This is especially the case with the rough systolic pulmonary murmurs. In such cases the distinction must be made by other means. The pericardial friction sounds, being produced by the move- ments of the pericardial surfaces over each other, must evidently be heard through the whole period of the heart's action, and are not, like the endocardial murmurs, connected exactly with the moment of the closure of the valves, that is, with the systole and diastole. The friction sounds not only accompany the heart sounds, but are prolonged beyond them, are interposed, as it were, between them (Skoda), and may occupy the whole dura- tion of the cardiac movement. In the latter case, the ear often receives at first quite a confused impression, but intermissions can be detected, which remind one of the rhythm of the footfall of a galloping horse. Each side of the heart can produce a systolic and diastolic murmur of different durations, so that each beat of the heart may be accompanied by four murmurs. Most frequently three are heard, one presystolic, belonging to the systole of the auricles, and two longer sounds, corresponding to the systole and diastole of the ventricles.' Gerhardt has noticed a rare pericardial friction sound, which he describes as divided into several parts. It was heard by him in a case of complicated valvular disease, where the pulse had sunk to forty. Multipartite undulations were also observed in the jugular veins, and, synchronous with the undulations, a multipartite friction sound was heard to the outside of the aorta. The undulations and the friction murmur were supposed to be produced by the right auricle undergoing multipartite contractions2 before a ventricular systole occurred. When the friction murmur occurs only at the time of the systole or of the diastole, it is generally prolonged beyond the cardiac sounds; if it be exactly synchronous with these sounds it is usually very difficult to determine absolutely its pericardial character. The pericardial friction sounds, moreover, frequently present 1 Traube, Ges. Abhandlungen. 2. Bde. 2 Lehrb. der Auscultation und Percussion. VOL. VI.—38 594 BAUER.—DISEASES OF THE PERICARDIUM. the peculiarity of being altered by the respiratory movements, there being almost always an increase of the sound during inspi- ration. A similar result occurs also in endocardial murmurs, but very rarely; these usually remain unchanged or decrease in intensity. The inspiratory increase of the pericardial sounds is probable due to the greater friction between the opposed sur- faces of the pericardium, occasioned by the contraction of the diaphragm. Another important feature of these sounds is the effect pro- duced by changing the position of the patient, this procedure, where the lesion is circumscribed, causing their appearance or disappearance. When, in consequence of effusion, the sound has been lost, it will frequently become audible again if the patient be made to sit upright or to bend his body forwards. Some- times also, if the chest be elastic, forcible pressure with the stethoscope will develop or increase the sound,1 but if the pressure be too forcible, the movements of the heart, and at the same time the friction, are enfeebled (Friedreich). According to Gerhardt, the abstraction of blood sometimes increases the intensity of the friction sounds, sometimes dimin- ishes it (through absorption of the exudation, or weakening the cardiac movements r(). Under some circumstances the sounds seem very superficial, as if heard directly underneath the ear; but this is the case only when they originate in the superficial cardiac region, (where the heart is not covered by lung tissue), and then the impression re- sults rather from the strength than from the proximity of the sound. On the other hand, friction murmurs, particularly the more feeble ones, are often confined to a very limited space, while the endocardial murmurs, except perhaps the presystolic mitral murmur, are generally audible over a larger surface. Sometimes, though rarely, a strong friction murmur can be felt. Occasionally it is so loud that the endocardial sounds can no longer be recognized, and are completely concealed. In such cases it is important to auscultate the carotid, where the trans- mitted aortic and pulmonary sounds can usually be heard. This fact was doubted by Skoda, but without good reason. PERICARDITIS.—PHYSICAL SIGNS. 595 Not only is pericarditis frequently combined with endocar- ditis and valvular affections; but aside from this connection, it may itself give rise to endocardial murmurs.1 Thus adventitious systolic murmurs are sometimes observed at the mitral orifice, and still more frequently at the origins of the vessels, particularly the pulmonary artery. Generally these vascular murmurs are due to the usual cause, but it is probable that in some cases they are produced by the pressure of the effusion upon the walls of the vessels. Cejka has noticed a disappearance of the first aortic sound, and explains it by an inflammatory relaxation of the portion of the arterial wall covered by the pericar- dium. A division of the second vascular sound, as frequently observed by Skoda, has no diagnostic significance. The equalization of the intervals between the cardiac sounds—the so-called pendulum rhythm, as Roger calls it—is at least of infrequent occurrence. When a copious effusion into the pericardium has taken place, the cardiac sounds and endocardial murmurs may become feeble or entirely disappear. Sometimes this is the case only when the patient is lying down, the sounds returning in the upright posi- tion, or on bending so as to throw the heart forwards. Usually the sounds are merely weakened; a complete disappearance is very rare. Under such circumstances the force of the pulse is often found to be disproportioned to the feeble sounds of the heart. If the separation of the opposing pericardial surfaces (anteri- orly) be slight, or wholly prevented by the occurrence of agglu- tinations or adhesions, the cardiac sounds will still continue to be audible over this region. The pericardial friction sound may be confounded not only with endocardial murmurs, but also with the pleural friction sound produced on the external surface of the pericardium by roughness of the pericardial pleura or of the opposing pleuritic surface. This sound is called the extra-pericardial, pneumo- p<-/'('cardial, or pleuro-peri car dial friction sound. 1 As has been observed by Latham and Hughes. 596 BAUER.—DISEASES OF THE PERICARDIUM. A. Ferber has recently, in his work on Pleuritis,1 carefully investigated this form of friction sound. According to his observations, it is heard most frequently in the neighborhood of the apex of the heart, that is, near the tongue-shaped lobe of the lung and the almost triangular complementary fold of the pleura lying in front of the heart; more rarely it is heard along the sternum, as high as the third or second rib, where the median borders of both lungs are situated. Usually in such cases two sounds can be distinguished, one connected with the respiration and the other with the movements of the heart. The friction sound produced by the cardiac movements is modified in several different ways by the respiration, be- coming more distinct on superficial breathing, while the portion of the sound con- nected with the inspiration is frequently increased by moderately strong respira- tion. When the breath is held, the sound disappears immediately or after a few beats of the heart; but it may also continue during the entire respiratory pause, or, after a partial disappearance, return. A. Ferber thinks the sound may be produced in two ways, according to the situation of the roughness, either by the friction of the roughened pleura against the pericardium or by the friction of the roughened pericardial pleura against the opposing pleural surface. The influence of the suspension of breathing depends upon the action of agglutinations, which prevent the systolic impulse of the heart from producing any rubbing until a strong respira- tion breaks up the adhesion.2 The extra-pericardial nature of the friction sound is indicated with certainty when a suspension of breathing has the effect oi diminishing the intensity or of immediately arresting the sound. If it continues unaltered through the respiratory pause, a dis- tinction is impossible. Some other respiratory sounds are liable to be confounded with endocardial,' but not with pericardial murmurs. I recollect, however, one case in which there was a dry, crackling systolic rale near the apex of the heart, sounding very much like a pericardial friction sound. The frequency and quality of the pulse during the course of pericarditis are modified by so many causes, particularly by the occurrence of complications, that the pulse cannot be said to present any distinctive character. In fact, rules are impossible. There are probable indications, however, which it may be well to 1 Die physicalischen Symptome der Pleuritis exsudat. Marburg. 1875. 2 For particulars in regard to this form of friction sound, see article on Pleuritis; also A. Ferber, 1. c. 3 See Kuessner, Beitr. zur Kentniss d. accid. Herzgerausche. Deutsch. Archiv f. klin. Med. XVI. 1. 19. PERICARDITIS.—PHYSICAL SIGNS. 597 consider, because in many respects, especially as regards the condition of the heart, the examination of the pulse affords information of the greatest importance. It is not uncommon for pericarditis to run its course without any considerable acceleration of the pulse. Thus, we often see pericarditis occurring in connection with articular rheumatism, without any further increase of the pulse ; but where the patient has been much reduced beforehand, the complication, as a rule, exerts an accelerating influence. During the first few days of the disease the pulse is often temporarily accelerated, so as to run up to one hundred or one hundred and twenty; but this initial acceleration usually sub- sides within a short time. It is commonly ascribed to an irrita- bility of the heart, induced by the inflammation of its serous coat; that is, the inflammation exerts an accelerating influence upon the cardiac muscle or the excito-motor ganglia. Yery frequently it is noticed that a slight bodily exertion is sufficient to produce a considerable increase in the frequency of the pulse. A continuous acceleration may be due to quite a variety of causes, among the most important of which are n^ocarditis and degeneration of the muscles, lesions which usually induce other changes in the pulse besides an increased frequency. The acceleration of the pulse may depend also upon elevation of the temperature and upon respiratory and circulatory disturbances. The rhythm may also be changed, but this occurs less fre- quently than some former observers have stated. Thus, Gendrin has asserted that he has observed alterations of rhythm in eleven out of fourteen cases, and Louis in about half ; according to Bamberger, however, this symptom is not so frequent, and usually occurs only temporarily at the outset of the disease, and the same opinion is expressed by Nothnagel.1 The alteration may consist either of an irregularity or of a simple intermittence of the pulse. When the symptom occurs during the latter part of the disease, it frequently depends upon disease of the cardiac muscle. In other cases, and particularly in the initial stage of the disease, the irregularity may be occasioned by the excitation 1 Ueber arhythmische Herzthatigkeit. Deutsches Arch, fiir klin. Med. XVII. 2 u. 3. 598 BAUER.—DISEASES OF THE PERICARDIUM. of the inhibitory nerves induced by the inflammation. In a particular case, however, it is hardly possible to decide whether the chief share is taken by the muscular elements, by the musculo-motor ganglia, or by the inhibitory fibres. A special form of pulse, the pulsus paradoxus, will be considered some- what more fully at the conclusion of this chapter. Great differences prevail also in regard to the tension of the arterial system and the height of the pulse-waves. In many cases no change is noticed. At the outset of the disease, cor- responding to the more forcible action of the heart, the tension may be increased, and the pulse extraordinarily full. If the filling of the ventricle be interfered with by the occurrence of copious effusion, or if the muscle have undergone important changes, the tension falls and the pulse-waves become very low. In the first instance, if the apex-beat can still be felt, a striking disproportion is often noticed between the action of the heart and the pulse-waves ; in the latter case the pulse is frequently also irregular, and over the heart itself we meet with the changes which belong to degeneration of the organ (feebleness of the apex- beat and cardiac sounds, systolic murmurs, etc.). Retardation of the pulse occurs but rarely during the course of pericarditis ; now and then, however, it occurs as an after- symptom, and is then generally due to exhaustion of the cardiac muscle. That such a fatigue may occur without any consider- able lesion of the muscular substance, and may of itself in- duce paralysis, cannot at present be denied, although no proof on this point can be obtained during life. Recovery is possible even in inflammatory and degenerative processes, and is no evi- dence therefore that the condition was one of simple exhaustion. Traube has recently called attention to the fact that in some cases of copious pericardial effusion the left carotid and radial arteries are smaller and pulsate less forcibly than the corresponding arteries on the right side. He is unable to give a full explanation of this symptom, but he regards it as certain that it must be ascribed to the effusion.1 The effusion exerts upon the external surface of the heart a pressure proportioned to the amount of fluid and to the lateral 1 Charite-Annal. 1874. PERICARDITIS.—PHYSICAL SIGNS. 599 resistance resulting from the tension of the pericardium. The share taken by each of these two factors will of course differ considerably in particular cases, according to the varying quan- tity of effusion, and to the thickness, thinness, or elasticity of the pericardium.1 The systole of the auricles and ventricles is not restrained by the effusion in the pericardium.2 During the con- traction of the heart the intrapericardial pressure must be diminished. The pressure weighing upon the heart may, how- ever, interfere with the diastolic movement, and thus lessen the flow of blood into the cavities. This mechanical influence of the effusion is felt chiefly upon those portions of the heart which, in consequence of their membranous character, are less resistant to pressure, viz., the auricles. The diastolic relaxation of the cardiac cavities, particularly the auricles, and the filling of the same with blood, are assisted normally by the vis a tergo of the venous blood as it pours into the auricles, and by the elastic traction of the lungs. These two forces are directly opposed by the pressure of the pericardial effusion. Moreover, the traction of the elastic and tense lungs upon the walls of the heart is diminished in cases of pericardial effusion, because the lungs are themselves compressed, and there- fore lose a part of their tension. A large effusion may also exert pressure upon the large ves- sels where they lie within the pericardial sac, and thus interfere with the filling of the aorta and pulmonary artery. Inflammation of the pericardial layer of the large vessels within the pericardial sac seems to be a rare occurrence. When it does occur, it may lead ultimately to such lesions as thickening, diminished contractility, and even dilatation. When the veins are unable to discharge their blood into the auricles in the normal manner, over-distention of the veins in the general, as well as the pulmonary, circulation naturally re- 1 The lateral pressure of the effusion in the pericardium can, to be sure, be esti- mated manometrically in the cadaver, but the conlitions are so much altered by death that the figures obtained in this way would be of little direct service. 3 In Traube's opinion the systolic motion of the heart is greater in pericardial effu- sions than under normal circumstances, because the fluid opposes less resistance to this movement than do the membranes where they fit close to the heart in the normal man- ner. Berl. klin. Wochenschr. 1872. 7. 78. 600 BAUER.—DISEASES OF THE PERICARDIUM. suits, while the filling and the pressure in the aortic system is diminished. Under such circumstances the veins in the neck are found to be swollen, and to present undulatory movements; in high degrees of stasis the distention is very marked, and sometimes a true venous pulse is noticed (Stokes, Friedreich, and others). This venous congestion may lead also to passive hyper- aemia as well as to catarrh and oedema of the lungs, to more or less cyanosis, and finally to oedema of the extremities and gen- eral dropsy. Other results also make their appearance, such as headache, vertigo, enlargement of the liver, gastric and intes- tinal derangements, and of course also various symptoms due to a defective supply of oxygen to the tissues. ■ The swelling of the cervical veins is a comparatively frequent symptom, and is, as a rule, accompanied by multipartite undulatory movements. The occurrence of a true venous pulse, without tricuspid insufficiency, was demonstrated by Fried- reich in one case of pericarditis. This observer, as is well known, distinguished two forms of venous pulse, one a more marked form, associated with tricuspid insufficiency, and the other a slighter variety, in which the faulty closure occurs with the valves of the veins and not with the tricuspid. According to Skoda, the venous pulse in large pericardial effusions is produced in the following way: the motion communicated to the fluid by the ventricular systole is transferred to the auricle as the most yielding part, while the expansion of the auricle is hindered by the effusion. This explanation is, however, unsatisfac- tory ; the venous pulse is formed here just as it is under other circumstances. The highest degrees of stasis and derangements of circulation may be produced by large pericardial effusions, but in most cases they are due chiefly to some affection of the cardiac muscle itself, while the effusion serves to increase still more the results of the imperfect force of the heart. The occurrence of derangements in the nutrition of the cardiac muscle may manifest itself by the diminished fulness of the pulse—the pulse-waves becoming small, and not unfrequently also irregular and intermittent, and the in- crease of tension at the time of the ventricular systole becoming less marked. In the presence of cardiac changes like those described, it is usually noticed that the cavities of the heart become dilated. This result is frequently absent, however, when the pericardial effusion is abundant; on the contrary, the heart is found to be strikingly small, notwithstanding the marked degeneration of the muscle, obviously PERICARDITIS.—PHYSICAL SIGNS. 601 on account of the pressure of the fluid upon the wall of the heart and the imperfect filling during the diastole. This condition cannot be recognized by physical signs during life on account of the fluid accumulation. Sometimes the symptoms of weakness of the heart make their appearance very rapidly; attacks of sudden loss of power in the heart may also occur, with an almost imperceptible pulse, and death may ensue in an attack of this kind. These symptoms of cardiac exhaustion are of course not peculiar to pericarditis ; they occur in like manner in diseases of the cardiac muscle arising from other causes. The derangements of respiration, which are sometimes noticed during the course of pericarditis, are not to be regarded as always directly due to the pericardial inflammation. Severe pains in the chest and epigastrium may induce an acceleration of the breathing. On the other hand, the mechanical effect of the effusion, as well as disease of the cardiac muscle during the course of a pericarditis, may give rise to serious respiratory disturbances, and in fact to the highest degrees of subjective and objective dyspnoea. Although the effects of the pressure of the pericardial effu- sion upon the heart have, no doubt, been frequently exaggerated, yet there can be no question that under favorable circumstances the circulation may be considerably deranged in this way, and that the interference thereby produced in the exchange of gases, may even lead to severe dyspnoea. Still another agency in the production of dj^spncea is the compression of the lungs, or of the left bronchus, by the pericardial effusion. In such cases the respirations are frequent, deep, and markedly dyspnoic, the accessory respiratory muscles are tense, the alas nasi play, the patient becomes very cyanotic, cold, and collapsed, and the skin is covered with a clammy sweat. Very often there is exquisite orthopnoea. The difficulty of breathing is usually most intense in the recumbent posture, and it is easier for the patient to lie on the left side than on the right. Zehetmayer saw one patient, with a large pericardial effusion, who was able to breathe only when supported on his hands and knees. Patients also experience great distress and restlessness, and suffer unspeakably from a sense of oppression and craving for air. The orthopnoea, in cases of pericardial effusion, is specially due 602 BAUER.—DISEASES OF THE PERICARDIUM. —in addition to the usual causes—to the fact that the mobile fluid lies more unfavorably in the horizontal position of the body than in the sitting posture. In the latter position, especially if at the same time the body be bent forwards, the effusion sinks forwards and downwards ; while in the recumbent posture it presses up- wards and backwards, so as to exert considerable pressure upon the auricles and origins of the large vessels. Moreover, the pres- sure upon the lungs is greater in this position, and, for the pur- pose of avoiding this effect upon the right lung, the patient pre- fers to lie upon his left rather than upon the right side. In many cases the respiratory disturbances are still further increased by the presence of a dry cough, with a mucous, frothy expectoration. Sometimes there is said to be a paralysis of the diaphragm, producing a retrac- tion of the epigastrium on inspiration. This has been explained partly by the pressure of the distended pericardium upon the diaphragm, and partly by the extension of the inflammation. The general condition of the patient is also of importance as regards the appearance of dyspnoic symptoms, for in the anaemic the dyspnoea is less severe than it is in those who are well nourished ; the same is also true of the rapidity with which the exudation and consequent obstruction appear, according to the well-known saying, that the more acutely a disturbance begins the more severe will it be.1 If the heart itself undergoes a considerable disturbance of nutrition in consequence of the inflammation of its serous envelope, this myocarditis or myodegeneration, with the conse- quent weakening of the power of propulsion, and the disturbance of the circulation, may lead to intense dyspnoea, and if, in the course of an uncomplicated pericarditis, severe dyspnoea and diminution of the aeration of the blood appear, they are much oftener due to an affection of the heart itself than to the mechanical results of the exudation. The disturbances of respir- 1 This is analogous to the well-known experiment, according to which an animal dies in an atmosphere containing a certain amount of carbonic acid, if it is suddenly compelled to breathe in it, while it will survive if the air is brought gradually to contain the same amount of the gas. PERICARDITIS.—PHYSICAL SIGNS. 603 ation which arise in such a way behave exactly like those which occur in the course of other heart diseases ; a more abundant exudation into the pericardial sac would naturally tend to add to the symptoms. In many cases the dyspnoea, anxiety, and oppression seem to be purely nervous manifestations, due to irritation of the branches of the pneumogastric. Irregularity, also, acceleration of the movements of the heart, stenocarditic attacks, are thought to be due to the influence of the inflammation upon the regula- ting nerves of the heart in their course. During the attacks of dyspnoea violent vomiting sometimes occurs, together with tormenting, painful singultus. The latter symptom might be explained by an inflammation of the phrenic nerve passing down over the pericardium. In rare cases the patients complain of a painful and convulsive feeling in the throat and oesophagus, and of dysphagia. The dysphagia may be caused by the direct pressure of a large exudation upon the oesophagus ; in other cases it seems likewise to be a symptom of irritation, for it has also been found when the exudation was small. Double paralysis of the vocal cords, occasioned by the pres- sure of a large pericardial exudation upon both recurrent nerves, was observed by Baeumler. The voice returned after the exuda- tion was absorbed. On account of the rarity of this symptom Baeumler1 thinks that it may require the cooperation of several forces, and that the great venous congestion in his case may have had some influence, especially upon the paralysis on the right side. Some nervous attacks, especially fainting-fits, also convulsions, maniacal attacks, delirium, sopor, which were regarded by the older physicians as frequent and characteristic symptoms of pericarditis, are due not to it but to disturbances of the circulation in the brain, cerebral oedema, or other complications. Only seldom is there such a concurrence of circumstances in the course of a pericarditis that symptoms of this kind are observed. Corvisart mentioned the purulent breaking down of the bulb of the eye, sometimes appearing suddenly, as a symptom of pericarditis. Friedreich adds to this observa- tion that the symptom is due not to pericarditis, but to endocarditis and embolism of the arteria ophthalmica. 1 Deutsches Arch. f. klin. Med. Bd. II. S. 550. 1867. 604 BAUER.—DISEASES OF THE PERICARDIUM. Bouillaud expressed the opinion that no painful symptoms accompanied pericarditis, and that when such were present they were due to pleuritic complication. This view is decidedly incorrect, for there are cases, especially of spontaneous pericar- ditis, in which a very characteristic group of abnormal sensa- tions is present. There are, however, many cases in which all pain is lacking, and others in which it is very slight, or promptly disappears again, so that the patients do not complain of it. A few transient stitches may be felt in the region of the heart. Many patients complain only of a dull pressure upon the breast, or of the sensation of weight and tension, of a load over the heart. In many cases a moderately intense stabbing or pressing pain is felt for some time in the neighborhood of the heart, under the sternum, and may be increased, especially by the respiratory movements, but also by those of the body, by pressure over the heart and by percussion. A notable sensitiveness to pressure in the intercostal spaces occurs rarely. According to the observations of Baeumler and Gueneau de Mussy, pain is experienced in the epigastrium more frequently than in the region of the heart, and this pain is spontaneous and occurs also upon pressure ; the latter is indeed the more common. The epigastric pain can also be increased by respiration and move- ments of the body, so that dyspnoea and inability to walk result; the movements of the heart can also increase it. According to Gueneau de Mussy, sensibility to pressure in the epigastrium is found especially at the angle between the ribs and the ensiform process, sometimes on the left, sometimes on the right side. Pain between the lower insertions of the left sterno-cleido- mastoid muscle—sensibility of the trunk of the phrenic nerve which is involved in the inflammation in consequence of its ana- tomical relations with the pericardium—is less frequently present at the same time with that in the epigastrium. The pain may radiate from that point, especially towards the left shoulder, but also along the whole of the left arm and towards the left ear. Baeumler also noticed painful sensibility of the left side of the larynx increased by every movement of the heart. PERICARDITIS.—PHYSICAL SIGNS. 605 The pains about the heart and in the epigastrium may also radiate in different directions, to the right side of the thorax, the back, and the abdomen.1 Tliese subjective symptoms appear in many acute cases at the beginning of the inflammation, and precede the objective changes; in other cases the latter appear first after a friction murmur has existed for some time. The feeling of palpitation of the heart is not unfrequently complained of, and in fact, under certain circumstances, painful palpitation may be felt. The friction murmur is comparatively seldom perceived by the patient. Sleep is often disturbed, especially when the above-mentioned painful sensations are present. The head is usually free or but slightly affected. Severe brain symptoms do not belong to pericarditis, but to consecutive or complicating circum- stances. The ultimate changes which the secretion of urine undergoes in consequence of pericarditis depend upon the height of the temperature of the body, upon the amount of liquid exudation into the pericardium, and upon the effect which in some cases the pericarditis has upon the aortic pressure. Moreover, the fundamental disease must of course be taken into consideration, whether it is combined with high fever, abun- dant perspiration, exudations elsewhere, albuminuria, etc. In the majority of cases the amount passed in twenty-four hours is considerably below the average, the specific gravity is increased, it is rich in coloring matters (relatively, and also ab- solutely in many cases), and a brick-dust deposit is often thrown down on cooling ; for at the temperature of the body, the urine being diminished in quantity, becomes saturated with the urate 1 The pericardium normally possesses only a slight degree of sensibility; compare Zuckerkandl, Sitzungsber. der Wiener Akad. 1870. LXII. 1. 151. et seq. This author found branches of the pneumogastric of considerable size, varying in number and points of origin, which came from the oesophageal or posterior pulmonary plexus, and were distributed mainly to the posterior wall of the pericardium. The pericardial nerves arise, first, from the pneumogastric; second, from the phrenic, especially those of the anterior and lateral walls; third, from the sympathetic, with fibres from both inferior cervical ganglia. 606 BAUER.—DISEASES OF THE PERICARDIUM. of soda. Nothing definite is known as to whether the different products of secretion suffer any qualitative or quantitative change, but, according to F. Heller, it is thought that the chlorine compounds, as in other exudative processes, are greatly dimin- ished ; as the previous conditions, however, were not exactly known, these investigations cannot be relied upon. Of the known factors which contribute to the reduction of the secretion of water through the kidneys, several, as a rule, act together. The lessening of the pressure in the aorta, in con- sequence of the diminished power of the heart, has the greatest influence. The obstruction to the flow of the blood which results leads to the development of congested kidney, and therewith to albuminuria. Even without pronounced congestion, albumen may appear in the urine, rarely as a febrile symptom, more often as the expression of an already existing or complicating disease of the kidneys. General rules cannot be laid down with reference to the be- havior of the fever, for in most cases it is secondary. If the primary disease is an acute febrile one, a further rise of tempera- ture may or may not be associated with the appearance of peri- carditis. If the pericarditis first appears while the fever of the primary affection is going down, it is often the case that a new rise of temperature does not occur. Inflammation of the peri- cardium occurring in the course of chronic affections sometimes begins very acutely with a chill and high temperature ; in other and very numerous cases it comes on insidiously, without any rise of temperature. Spontaneous pericarditis, also, simulating an acute affection of the chest, may show high fever with an initial chill, or, still more frequently, without any ; this is espe- cially the case when strong, previously healthy, individuals are suddenly attacked by pericarditis. On the other hand, when the disease is developed slowly, in feeble and old people, it often happens that its entire course is free from any rise of temperature. If fever is present it often disappears when the exudation has reached its maximum, and perhaps reappears, during absorption, as a slight increase of temperature. When the exudation is purulent, fever is always present, at least tem- porarily. PERICARDITIS.—DIAGNOSIS. 607 Diagnosis. To distinguish inflammatory effusion into the pericardium from hydro-pericardium, we have a number of distinctive signs which, in the majority of cases, render it possible to discriminate the one from the other. There is no difference on percussion, or at the most, it may be remarked that the distention of the pericar- dial sac by a serous exudation may become enormous, greater than it is in most cases of pericarditis. On the other hand, a friction murmur is never present with a serous exudation. Furthermore, all inflammatory and febrile symptoms are lacking, while they are present, frequently, at least, in pericarditis. The consideration of the etiological conditions, which usually declare plainly for one or the other, is very important. The diagnosis of the character of the exudation is very difficult and generally is only a probable one. There are no certain dif- ferences in the physical signs l and we can do little more in this way than determine approximately the quantity of liquid. The nature of the primary affection and the individuality of the patient furnish some useful means for determining whether the exudation is sero-fibrinous, or hemorrhagic, or purulent. Experience teaches that the pericardial exudation in feeble and cachectic individuals, especially with the so-called hemor- rhagic diathesis, is very often hemorrhagic; this is especially true of scurvy, morbus maculosus, variola, and scarlatina hem- orrhagica. There is the more reason to suppose a hemorrhagic effusion if with its appearance the patient becomes suddenly and visibly anaemic, which always presupposes a considerable loss of blood. In tuberculous and carcinomatous individuals also the exudation is not unfrequently hemorrhagic, but hemorrhages may also take place into the effusion in individuals who were previously quite healthy, and without the aid of any severe 1 An intense, widespread friction murmur lasting for a long time with slight increase of dulness is certainly to be expected with a fibrinous exudation, and, on the other hand, we may look for a large area of dulness and a slight temporary friction murmur, when the effusion is mainly serous. The fever also is often quite high when the exudation is more fibrinous. These diagnostic signs are very uncertain, although theoretically they appear correct; but manifold complications do not permit so simple a distinction. 608 BAUER.—DISEASES OF THE PERICARDIUM. general disease. As a rule, however, a sure diagnosis is not possible. The diagnosis of purulent exudation usually offers great diffi- culty. It may be suspected in pyaemic affections, for there the pericardial exudation is generally purulent; in other grave general diseases it occurs not unfrequently. Leaving out of consideration those processes whose course is marked by violent symptoms, and in which the appearance of pericarditis usually hastens the catas- trophe, there are purulent processes, in the neighborhood espe- cially, which set up inflammation of the pericardium with forma- tion of a purulent exudation. Furthermore, we often find puru- lent exudations in those cases which take on a chronic character, and in which, temporarily at least, febrile symptoms of a moderate degree usually appear. In such cases the symptoms of disease of the muscular tissue of the heart also appear with especial fre- quency and severity. The opinion, that the friction murmur is often absent in purulent pericarditis, seems to me to be erroneous. The murmur often disappears, but only after it has lasted for a long time, and in consequence of the adhesion of the pericardial surfaces to each other. Ichorous exudations occur rarely, and can only be suspected when there are neighboring abscesses or general septic processes, such as endocarditis diphtheritica, and others. A process of this kind is indicated by no local symptom ; only in exceedingly rare cases do we have a pyopneumo-pericardium. The severe general symptoms in such cases, the high fever, the frequent thready pulse, delirium, and rapid collapse belong to septicaemia. As for the physical signs of pericarditis, similar physical changes under other circumstances may of course lead to mistakes. The increased dulness of the pericardium may be confounded with enlargement of the heart depending upon dilatation and hypertrophy. The shape of the area of dulness is characteristic enough, at least if the exudation is abundant. The dispropor- tion also between the increased area of dulness and the feeble apex-beat, which is entirely lost when the patient lies upon his back, and is also perhaps overlapped by the dulness on the left, together with the slight heart sounds and the absence of valvular murmur, indicates a pericardial effusion. PERICARDITIS.—DIAGNOSIS. 609 The spreading and increase of the area of pericardial dulness under the eyes of the observer is very significant. It is true that this may occur rapidly in consequence of dilatation of the ventri- cles, and thus be mistaken for a moderate pericardial effusion. But acute enlargement of the ventricles most frequently affects the right side of the heart, and consequently the area of dulness seems only to be broader. Such a dilatation of the ventricle must also have a definite cause, which could scarcely escape detection. Uncovering of the heart by retraction and collapse of the lungs would be made clear by the shape of the area of dulness, by the elevation of the diaphragm, and by the effect upon the dulness of the shifting of the edges of the lungs during inspira- tion. If, on the other hand, the uncovering is due to connective tissue adhesions, the area of dulness is but slightly changed by inspiration, and at the same time the area of relative dulness does not show an increase corresponding to that of absolute dulness. On the other hand, the edges of the lungs may be so fixed that even when there is a pericardial effusion they cannot be pressed back. In such cases the area of absolute dulness is not increased, but that of relative dulness is. The diagnosis becomes much m©re difficult when there is emphysema of the lungs. The presence at the same time of an effusion in the left pleural cavity may add some difficulties to the diagnosis, especially if the pleuritic effusion fills the anterior portion of the thorax so that the upper and left outlines of the heart cannot be distinguished, and the organ itself is shifted to the right. In such cases the distinctness of the heart sounds on the right of the sternum is important to this extent, that it indicates displacement of the heart. It certainly happens very seldom that the edges of the lungs are empty of air at such points and to such a degree that the area of dulness resembles that of a pericardial effusion. This may be caused somewhat more often by encapsulated pleuritic effusions or by pleuritic membranes. Mediastinitis also can cause a similar dulness by the deposit of an exudation on the posterior surface of the anterior wall of the thorax. In all these cases the vesicular respiratory murmur, which is present with VOL. VL—39 610 BAUER.— DISEASES OF THE PERICARDIUM. pericardial effusion, is absent over the area of dulness. Fremitus and the movability of the edges of the lungs all furnish important distinctions. Mediastinitis is very rare, and is usually the result of a traumatism, of disease of the sternum, or of the ribs, or of the burrowing of pus downwards from the neck. With aneurism of the aorta or tumors of the mediastinum, the dulness may exceptionally have the form of the pericardial triangle, and as in both cases other characteristic signs may be absent, a mistake may easily be made. The following case, from v. Ziemssen's Clinic, is an example of the kind : A man, forty-nine years old, came on the 18th January, 1870, to the surgical clinic to be treated for a tumor on the left forearm, which had first been noticed in 1870 as a small knot, and which in the subsequent interval had grown to the size it then had. The patient, in consequence of loss of strength and severe dyspnoea, was in a condition which made an operation impracticable, find he was therefore sent to the medical clinic. The difficulty in breathing began early in December, 1875. A tumor on the left forearm, chiefly on the flexor side, extending from the upper third to the wrist, increasing anteriorly, and largest at the wrist, covered with a glistening skin traversed by large veins. A few knot-like prominerc s of soft fluctuating consistency. The consistency of the rest of the tumor was firmer. The muscles were involved in the tumor. Flexion and extension quite feeble. The upper arm and hand are unaffected. The cubital, axillary, and sub-clavicu- lar glands are not swollen. Appearance anaemic, voice weak, considerable emaciation. The patient cannot lie at all upon the left side, and for only a short time upon the right; pronounced orthopneea. Respiration frequent, costal and very dyspnoic; the epigastrium scarcely moved at all; no cyanosis, no swell- ing of the veins in the neck. An area of dulness upon the anterior thoracic wall, of the shape of the distended pericardium; the blunt angle of the triangle reaches to the clavicle, and is quite broad, the left border extends down from the left axilla, the right one runs along the right side of the sternum, and unites at the third rib with another area of dulness. In the right anterior region, relative dulness begins at the lower edge of the third rib, and absolute dulness at the lower edge of the fourth rib, extending towards the axilla and down to the normal boun- daries. These limits change but slightly on inspiration, and the same is also true of most of the points of the triangular area of dulness. On changing from the recum- bent to the sitting posture and bending the upper part of the trunk, the absolute dulness on the right side shifts a very little upwards. The triangular area also is slightly affected by the change of position; the right border alone is somewhat nearer the sternum when the patient is lying down. Posteriorly on both sides is a hand's breadth of dulness, which can be somewhat displaced. The apex of the left lung slightly dull, especially posteriorly towards the vertebral column. On the right PERICARDITIS. —DI AONOSIS. 611 side, in front (R. A.), harsh, puerile respiration; on the left side, anteriorly (L. A.), undefined breathing with rhonchi, deep respiration slightly bronchial; left posterior superior region (L. P. S.) also undefined breathing; R. P. I. and L. P. I. feeble breath- ing, with many dull rales. R. A. in the region of the dulness the breathing is almost absent, and the same condition exists over the triangle. R. P. I. and L. P. I. the vocal fremitus very weak, and is likewise very much diminished in L. P. S.; in front and on the left side, it is stronger at the apex than on the right side; in L. A. in the region of the dulness, it is very weak; and on R. A. it is normal to the edge of the dulness, where it entirely disappears. Apex-beat nowhere to be felt, heart sounds very weak, and still more difficult to hear on account of the labored respiration. Spleen not enlarged. The lower border of the liver lies three finger-breadths below the ribs. Purulent sputum in considerable quantity, some of it brownish red and mixed with blood. Micro- scopical examination showed pus, blood, and some alveolar epithelium. Urine scanty, large deposit, very acid, no albumen. Temperature normal. The following diagnosis was made: effusion into the pericardium, perhaps due to new growths; a tumor in the right pleural cavity arising by metastasis from the cne on the left fore- arm; and also a double pleuritic effusion. The patient died on the 24th of January. Autopsy.—Body large, skin pale; a tumor on the left forearm, largest near the wrist. Both lungs adherent, especially at their anterior edges. An effusion of blood between the two pleural surfaces in the side of and behind the left lung. Scattered through both lungs encephaloid nodules, varying in size from a walnut to a child's fist, and containing extravasations of blood. The neoplasm crowds the mediastinum to the left, away from the lower and anterior border of the right lung, and causes it to cover the heart. The pericardial sac contains very little liquid. The surface of the heart covered with abundant stringy flakes; otherwise the heart shows no change. Liver normal in size, full of blood, evenly colored; the kidneys also full of blood, firm. The spleen flaccid, pale, measuring 10-J by 8 ctm. The mucous membrane of the stomach somewhat reddened, and showing small hemorrhages. The intestinal mucous membrane somewhat injected in places. Mesenteric glands unaltered. The tumor proved to be a sarcoma. As for the auscultatory signs of pericarditis, it was said, when speaking of the symptomatology, that in the majority of cases pericardial could be distinguished from endocardial mur- murs. Often the character of the murmurs and the moment at which they are heard are sufficient; the pericardial sounds are frequently delayed, and if they constitute a pure systolic-dias- tolic double murmur, the systole and diastole give the same impression of friction, while in the endocardial double murmur the systole and diastole are different. The point also at which the murmur is heard is of importance : the pericardial murmurs 612 BAUER.—DISEASES OF THE PERICARDIUM. are often heard at the origin of the great vessels and over the right ventricle, and then are not unfrequently quite circum- scribed. Change of posture, too, has much more effect upon the pericardial than upon the endocardial murmurs ; a murmur which can be heard only when the patient is in the upright posi- tion or lying upon his side is alwa}^s pericardial (Gerhardt). The possible means of distinguishing intrapericardial from extrapericardial friction have also been already mentioned. The diagnosis, whether and to what extent the muscular tissue of the heart is affected by the inflammation of the peri- cardium, can be based only upon such symptoms as are caused by myocarditis and myodegeneration, feebleness of the heart, weakness of the circulation and stasis, irregularity of the move- ments of the heart. It must, however, be remarked that not every irregularity in the action of the heart which occurs during peri- carditis, justifies the diagnosis of disease of the muscular tissue. Course—Terminations—Prognosis. As the intensity of the symptoms and the fundamental cause in pericarditis show great differences, so, too, is its course very irregular, and no rules can be laid down for the duration of the process. The whole process may terminate completely within a few days, as the cases of Baeumler and others show, though it is true that this can only happen when the effusion is not great. Even considerable sero-fibrinous exudations may be completely absorbed in the course of a few days, during which there is a no- table increase in the amount of urine, but the entire duration of the disease in those favorable cases is ordinarily from eight to ten days ; this is also usually the case in the course of polyarthritis rheumatica, pneumonia, and pleurisy, and in many idiopathic cases—much more rarely when preceded by primary disease of the heart. But even under these circumstances a longer course, one of from three to six weeks, is by no means an exception. The arrest of the inflammation, or rather of the exudation, is sometimes made known by a febrile attack ; if then absorption goes on rapidly, a slight elevation of temperature may be asso- ciated with it. PERICARDITIS.—COURSE—TERMINATIONS. 613 A fatal termination is very seldom the exclusive and imme- diate consequence of such a pericarditis, and happens only when the effusion is very large and when there are symptoms of dis- turbed respiration and circulation, dyspnoea, cyanosis, venous congestion, reduction of the arterial pressure. But as soon as we have to deal with feeble or old people, the conditions are changed and more unfavorable. In complicated cases, the kind of complication is of course of the greatest moment, since it is often more important than the pericarditis itself. Implication of the muscular tissue of the heart must be considered not merely as a complication, but rather as a result of the pericarditis. It may either appear acutely and cause death in the course of a few days, or it may lead to a chronic wearisome illness. On the other hand, death is caused often and promptly— within twenty-four hours—by scorbutic or hemorrhagic pericar- ditis, in which the effusion offers almost the characters of pure blood and may be very abundant, so that the loss of blood has much to do with the suddenness of the fatal termination. Thus a short time ago I saw a middle-aged man succumb to an idio- pathic pericarditis, in which the exudation had the appearance of pure blood and was very abundant. In contrast with sero-fibrinous pericarditis purulent inflam- mation may lead to death very rapidly before the exudation has become large. This is most frequently the case in grave general affections, such as pysemia, and then it is always a question how much is to be ascribed to the pericarditis. In other cases, in which the purulent condition of the exudation is dependent upon chronic constitutional or local causes, the course may be a very long one, but death is almost certain to result sooner or later. The importance and course of pericarditis due to chronic affections of the lungs, kidneys, and also the heart itself, may differ greatly ; every possible form of exudation and course may present itself. In general we can only say that in such cases every form of pericarditis may appear as the exclusive and direct cause of death. The gradual change into a chronic condition must be men- 614 BAUER.—DISEASES OF THE PERICARDIUM. tioned as a termination of acute pericarditis. This change is rare in rheumatic pericarditis, but more frequent in the idiopathic form, especially in chronic diseases of the heart and in chronic constitutional affections, in Bright's disease of the kidneys. After an acute period l the exudation remains stationary, or it may be in part absorbed, and then after a while poured out again, and thus the process drags along. Chronic pericarditis may grow out of an acute attack, or it may have this character from the beginning; recovery seldom takes place. Death usually results — sometimes suddenly, and in consequence of secondary myodegeneration, which is the almost inevitable result of chronic pericarditis. If life is preserved, absorption of the exudation goes on slowly ; there remain portionsa encapsulated between the pericardial layers; the abundant vegetations and the impermeability of the lym- phatics interfere with the absorption of the exudation. In such cases permanent lesions of the heart almost always result,—par- tial or general adhesion of the surfaces of the pericardium, degeneration and atrophy, dilatation and hypertrophy. After severe attacks and long duration of the disease, the signs of exudation may entirely disappear, while restoration of the muscular tissue of the heart follows slowly, and the symp- toms from that quarter still continue. This is more likely to be the case when the general nutrition has suffered during the disease and anaemia has been developed. Every bodily exer- tion causes oppression and palpitation, a condition which only gradually wears away. It is hard to say in how many cases, and under what circumstances in the various forms of pericarditis, complete restitutio ad integrum ensues, and in how many cases lasting changes remain. "We can only compare the frequency of pericarditis during life with the number of autopsies in which pathological changes of that nature are found. We can also arrive at some conclusion from the appearances presented at autopsies on the bodies of persons in whom during life pericarditis is known to have 1 If the exudation is purulent, a cheesj' collection and afterwards tuberculosis may result. 2 The term chronic, as applied to pericarditis, depends less upon the duration of the disease than upon the permanence of the symptoms or upon the appearance of inflam- matory relapses. PERICARDITIS.—COURSE—TERMINATIONS. 613 occurred, but from which they have recovered, and subsequently died from other causes. But we should be careful to exclude those cases of milk spots which appear to have arisen without any discoverable inflammatory cause. We have already remarked (p. 565), that doubtless even connective-tissue bands may subsequently be ruptured and absorbed. Loose spongy adhesions of this kind possibly may frequently be the result of a pericarditis, but firm and lasting adhesions of considerable extent are not often found as the result of a simple sero- fibrinous inflammation;l they usually arise where the course of the disease is pro- tracted, and absorption is delayed. More frequently, instead of adhesions, we find fibrous thickenings of the serous layers as the remains of a pericarditis, which how- ever cause no functional disturbances. The prognosis of pericaiditis must have been much more un- favorable in early times, when they were only able to recognize the more severe cases, and especially those associated with affec- tions of the heart itself, than now, when even the slightest cases come into the computation. Even Corvisart, Hope, Gendrin, and others considered pericarditis a very dangerous disease ; but Haclie, and especially Louis, showed that this view was incorrect. In one hundred autopsies of persons affected with pericarditis, Willigk found a cure had resulted in seventy-three; but here the milk spots were counted also. Duchek, in fifty-six cases of general pericaiditis, found twenty-seven cases (48.2 per cent.). Bamberger, in sixty-three cases, found thirty-seven (58.7 per cent.). Louis, in one hundred and six cases, found seventy (66.1).2 Naturally the prognosis varies greatly, according to the se- quence of events and the peculiarities which we have described under the "Course of the Disease;" but yet we are able to give a more accurate opinion in pericarditis, in some cases, than in many other forms of disease. First of all, we must consider the underlying cause of the pericarditis ; thus the pericarditis arising in the course of polyarthritis rheumatica has a very favorable prognosis. Yon Bamberger had not a single fatal case out of seventeen such, which he observed; and out of a great number of cases which I have seen, I have never yet seen one with a directly fatal result. So also those cases arising during attacks of pleuri- tis and pneumonia have a favorable prognosis, according to von 1 Duchek asserts that adhesions of the pericardial layers are found in ten per cent. of the cases in which recovery has occurred. 2 See Duchek, loc. cit. p. 07. 616 BAUER.—DISEASES OF THE PERICARDIUM. Bamberger. For idiopathic cases we cannot lay down any general rules, and the prognosis will be very varied. When there is heart disease already existing, a pericarditis will be regarded with suspicion. In all other cases the prognosis will be more or less unfavorable, according to the character of the primary disease.1 Beside the primary disease, existing complications will have more or less importance ; thus pleuritis, endocarditis, or even pneumonitis does not make tjie prognosis unfavorable, but simultaneous disease of the heart-substance renders it highly unfavorable: accordingly all symptoms which suggest such a condition should be carefully considered in forming a prognosis. The extent of the inflammatory process is also of importance, and a limited inflammation gives cause for anxiety only in cases where it complicates abscesses of the heart-substance, aneurisms, etc., and here on account of the primary disease, to which it possibly points. Moreover, the extent and character of the exu- dation is of weight, for large exudations cause much more danger than slighter ones. The prognosis in sero-fibrinous exudations is generally favorable, while in purulent it is bad, and in hemor- rhagic effusions the general constitutional symptoms and the quantity of the blood effused decide the question. So, likewise, the onset and course of the disease influence the decision; for nearly all cases which terminate in a cure run an acute course, while chronic cases offer very little encouragement. The age of the patient influences the prognosis very decidedly; infants of a year old usually die (Gendrin) ; in the later years of childhood the mortality is less ; and young adults show the least mortality. Beyond middle-life and in old people the prognosis again is unfavorable. The constitution also must be considered, for weak and broken-down patients succumb more frequently than those who are strong and well nourished. Duchek. is inclined, according to his statistics, to lay some stress on the sex of the individual, for the females showed a worse ratio of cures than the males. The prognosis will generally be rendered more difficult only in cases where pathological changes take place in the heart itself, 1 According to Latham, of patients with non-rheumatic pericarditis, ninety-one per cent. died. PERICARDITIS.—TREATMENT. 617 for those arise very acutely, but very insidiously, so that we may be suddenly and unexpectedly surprised by a failure of the heart's action. Whether or not the cure will be complete, we can only say approximately in the lighter cases, but not in the severe ones; indeed, some of the sequeke we cannot count upon, even after the cure of the disease ; these may occur later or not at all. (Such are hypertrophy, many cases of adhesion, etc.) Treatment. The objects to be attained in the treatment of pericarditis must be very varied, according to the character of the case, and quite opposite indications will arise ; for one case will require only a symptomatic and expectant treatment, while another must be attacked very energetically. Considering pericarditis in general as an inflammation of a serous membrane, our first indication would be to limit as far as possible the extent and amount of the inflammatory process. Of the antiphlogistic measures to accomplish this end, general blood- letting certainly is useless and at the same time dangerous, and it lias been generally abandoned. So, also, the employment of mercurial preparations, especially in the form of inunctions, although much extolled still by many physicians, has scarcely any influence that we can recognize on the course of pericarditis. We must at the outset confess that the end to be sought in our treatment is not a direct and immediate limitation of the inflam- matory process, which we cannot accomplish, but rather the control and arrest of important conditions which accompany it. First among tliese are derangements of the heart's function, and next pain and fever. To control the early increase in rapidity and force of the heart's action and also the fever, digitalis in large doses has proved itself a sovereign remedy.1 But a 1 The dose must be varied according to the strength of the preparation which is em- ployed, which is not the same in all localities. Here in Munich we need to give from thirty to forty-five grains to develop the full influence of the digitalis. It is given in powder, from fifteen to thirty grains divided over the twenty-four hours, or as an infusion with nitrate of potash or soda. 618 BAUER.—DISEASES OF THE PERICARDIUM. careful and strict watch is necessary on the part of the physi- cian that he may at once stop the remedy as soon as the digi- talis shows its full effect on the body and regularity of the pulse. The advantages to be gained in pericarditis by getting a quieter action of the heart are greater than would appear at first sight, and possibly the inflammatory process itself is thereby indirectly affected. The application of an ice-bag over the heart at the same time has been found to be very advantageous, whether in quieting the tumultuous action of the heart together with the sensation of palpitation, or allaying the pain which accompanies the disease. If the application is kept up uninterruptedly, it will most wonder- fully allay the pain, and is gladly used by most patients, and Lecognized as efficacious. At the same time the influence of cold upon the heart itself is advantageous. The employment of cold has been proved by others, as by Friedreich, to be useful, so that nowadays the moist and warm applications and poul- tices of former times, for this stage of the disease at least, are no longer used. If the pain is very severe, so that respiration is impeded, then a small dose of morpliine, either hypodermically or by the mouth, is clearly indicated, and is to be recommended in preference to local blood-letting; blisters we cannot recommend. To control the occasional sleeplessness, we may order morpliine, or a Dover's powder, or a dose of chloral, with benefit. As regards the treatment of the patient in other respects, above all we must secure complete rest of mind and body, and he should not be allowed to leave his bed. The giving of nourish- ing food in liberal quantities is usually prevented by a loss of appetite, or even disgust for food ; but still there is here no imperative demand to avoid the loss of bodily strength by crowd- ing the nourishment from the very outset. Accordingly, in the beginning, we might order a purely liquid diet, and in addition some acid drink—lemonade (drinks containing carbonic acid gas are by many physicians considered injurious). The bowels will be best regulated by enemata, or by some mild mineral waters. When we reach that stage where the inflammation is arrested, and the effusion remains at a stand-still, we must change oui PERICARDITIS.—TREATMENT. 619 treatment. If the effusion is not great and resorption begins properly, then no more active treatment is required. We lay aside the ice-bags, give more strengthening nourishment, and simply order the patient to lie quiet in bed for a time. If, on the other hand, the effusion is great, and does not begin to subside for several days after reaching its highest point, then we must endeavor to hasten its resorption. For this purpose we employ the various diuretics, digitalis in small doses to increase the arterial pressure, solution of acetate of potash, etc.1 Concerning the value of iodide of potassium for this purpose, I have no accurate information.2 In this stage of the disease good nourishment is very essential. If possible, the patient should not now lose any more of the elements which make up the body, buc rather add to them, for wo know how absorption of effusion is promoted by increased nutrition. The demand for albumen must generally be met by easily digested animal food, such as eggs, milk, and the like. The demand for non-nitrogenous food is probably less than normal, and we must give it in a variety of forms as it may be required. The patient may be allowed beer or light wine. Unfortunately the improvement of the nutrition cannot always be accomplished, for various reasons which we need not here discuss, and moreover our knowledge of the quantitative interchange of materials under these circumstances is very deficient. Sometimes the exhibition of preparations of iron and quinine may serve to assist in the improvement of nutrition, and also after the effusion has been absorbed, tliese remedies may be em- ployed to combat the existing anaemia. Besides causing diuresis, we ma3^ hasten the removal of the effused fluid by other measures—by derivation to the skin, ex- citing diaphoresis, and likewise by derivation to the intestines. Ph}Tsicians are divided as to how far we should rely on one or other of tliese methods, but at all events derivation to the skin is the one usually employed—frying blisters, and warmth and moisture (Bamberger), or, when the fluid has become purulent, 1 Of digitalis, for this purpose, we give doses of from eight to fifteen grains ; of the salts which cause diuresis by their affinity for water, acetate of jaotash is, according to my experience, the most efficacious. Of this I am in the habit of giving from sixteen to fifty-six grains, and as a rule the quantity of urine is thereby decidedly increased. s Waning Curran recommended veratrine, which he said caused a diminution of the fever, lessened the dyspnoea, and increased the quantity of urine. 620 BAUER.—DISEASES OF THE PERICARDIUM. continuous vesication, inunction with iodine ointment, or painting with the tincture of iodine, etc. The method by diaphoresis has in later days been somewhat neglected ; not wisely altogether, as it seems to me, for, in appropriate cases and with proper pre- cautions, I have found the use of hot baths and steam baths, with subsequent packing, of great advantage. When reabsorption of the effusion has occurred, and when the patient must be considered as really cured, we must advise careful and prudent living for some time yet, and, above all things, that he should shun severe bodily exertions and all things which call forth increased action in the heart (excessive use of alcohol, tobacco, etc.). If the circumstances of the patient permit, he should for the time have favorable surroundings (a trip to the country, etc.). The general principles for the treatment of an acute peri- carditis must often be variously changed or supplemented in given cases, according to the character of the primary disease, the presence of complications or specially dangerous symptoms, the nature of the material exuded, the course of the disease, and, finally, the peculiarities of the individual. In many cases of secondary pericarditis the conditions are such that we do not feel called upon to administer remedies for this morbid process; at most, we endeavor to arouse by stimu- lants the more rapidly failing power of the heart. Such a state of things is encountered in acute general diseases, and also in patients with phthisis or Bright's disease. From other, and indeed opposite reasons, many cases of articular rheumatism with pericarditis will not call for any change in treatment on account of this complication, since there are no subjective sufferings, and no important symptoms appear.1 In other cases, on the contraiy, especially with larger 1 In the use of salicylate of soda, in the treatment of articular rheumatism, a remedy has been introduced which certainly, as regards promptness of action, must be consid- ered an acquisition. As regards its influence upon the pericarditis, it cannot be doubted that, by completely cutting short the rheumatic attack, the occurrence of pericarditis will be prevented. But whether a pericardial inflammation once existing will be sub- stantially affected thereby, seems to me doubtful at least, with our present knowledge, even though the use of salicylate of soda may control the affection of the joints. TREATMENT. 621 effusions, I do not consider a thoroughly indifferent treatment warrantable, though I readily allow that even by that means we may obtain favorable results. The same holds true for the peri- carditis, which complicates a pneumonia or a pleuris3r, and espe- cially for that which arises in the course of an already existing heart disease. Moreover, it is to be remembered that in all cases in which, from the existence of a pneumonia, pleurisy, etc., the resistance to the circulation is very great, the utmost attention must be given from the outset to sustaining the powers of the heart, and every treatment calculated to weaken it must be avoided. Of the numerous individual symptoms, weakness of the heart in its various forms should be carefully considered. So soon as airy evidences of it appear, either in an acute or chronic form, the treatment must be essentially a strengthening one. The acute attacks of insufficiency of the heart, associated with very great anxiety, a feeling of oppression in the chest, and cold surface and extremities, call for the strongest stimulants: cam- phor internally or subcutaneousl}7, then ether, musk, and, above all, alcohol (brandy in the form of punch or champagne). If we want to accomplish anything under such circumstances, we must use our stimulants energetically and continuously. The only object in the use of stimulants is to sustain life during the momentary danger, and to support and improve the circulation for the time ; the heart itself will not be affected thereby. Permanent improvement must be sought first in nourishment, and especially in that containing large amounts of albumen. With this, digitalis, carefully given in small doses, will greatly assist, and also a continued use of alcohol (in the form of wine, not been*) will be found of service. If the process of degeneration of the heart has come on in a more chronic form and led to dropsy, the same principles of treatment hold good ; but here diuresis may be promoted and assisted by other measures, and in such cases hot baths and steam baths show excellent results. If patients of this kind suffer from distress for breath and are entirely sleepless, the use of chloral or morphine is, in my opinion, imperatively demanded ; also, the occurrence of hie- G22 BAUER.—DISEASES OF THE PERICARDIUM. cough or frequent vomiting may sometimes call for the use of narcotics. The nature of the exudation may call for careful consideration; this is especially so in the distinctly hemorrhagic form, as this declares itself by other special symptoms. Aside from the fact that in many cases of this kind the constitution demands a very strengthening treatment, we should make the attempt to arrest the bleeding by the application of ice-bags and the use of ergo tin. In the acute scorbutic forms Kyber has occasionally found excellent results from the use of large doses of quinine.1 The treatment of purulent effusions must in many cases be addressed to the primary disease; aside from this, our object will be to sustain the strength of the patient, and particularly to prevent any loss of power in the heart and to control the exacerbations of fever. Inasmuch as almost every treatment shows bad results, the question arises whether we should not attempt to procure an artificial emptying of the purulent exuda- tion by an operative procedure ; and here we may discuss the question whether the operation is permissible and what is its value in pericardial exudations generally. The operation, first proposed by Riolan the younger, was subsequently recom- mended by Senac, and also more recently by van Swieten, but was rejected by Morgagni and Corvisart—partly on account of the danger of the operation, and partly on account of the uncertainty of the diagnosis. The operation was first performed by Romero, in Barcelona, and with success (1819).2 Later, repeated attempts were nvide at paracentesis pericardii by Skoda and Schuh, and also by Kyber in scorbutic cases, and many times with favorable results. Trousseau like- wise recommended the operation. Aran carried out the proposal of Laennec, to throw in some irritating material into the pericardial sac, after puncture, to hasten the adhjsion of the surfaces, and with favorable results, although the operation had to bo repeated several times, on account of a renewal of the accumulation, in con- sequence of which air entered into the pericardial sac. Yet physicians were not wanting to condemn the operation, declaring it to be dangerous and not propor- tionately productive of good. It did not conie into general use, so that we cannot give a verdict based on practice. Very recently various physicians have repeated the operation, and especially in England it seems to have gained a firm foothold, where T. Clifford Albutt has particularly interested himself in it. T. H. Bartlett 1 M. Friedreich, loc. cit. 8 Friedreich, loc. cit. TREATMEXT. 623 has also published a case which was operated upon with favorable results, in which the aspirator was employed (drawing off fourteen ounces of bloody scrum).1 Experience thus far has taught us that the removal of pericar- dial effusions by an operation is not attended by any great danger, if ordinary precautions are taken. The results in accidental injuries of the pericardium support this view of the matter. The question therefore remains, how far does the operation accom- plish its object, judged by results ? and how should it best be performed ? Much that applies to the emptying of pleuritic effu- sions would be in place here. The number of cases operated on is as yet too small to be able to give a verdict as to the results of this method of treatment, and accordingly the indication for the operation is now confined to a narrower field than it perhaps will be later, when our experience shall have been enlarged. These indications are: immediate danger to life from the amount of the effusion, and the certainty of an unfavorable result from a stationary and particularly a purulent effusion. As regards the method of performing the operation, this, in the course of time, has been as varied as that of thoracentesis. Riolan and also Laennec proposed tre- phining the sternum. Probably we must here make a distinction between sero- fibrinous and purulent effusions, and we should doubtless select a capillary trocar and aspirator with exclusion of air (Potain) for the former, while in the latter the simple removal of the fluid would scarcely suffice for a permanent cure of the trouble. In the purulent form we shall have to establish an open wound with the opportunity of washing out the cavity, as has already been done. In the simpler operation with the capillary trocar and exclusion of air, we need not be very anxious about the exact spot where the puncture is made. We should insert the instrument in the fourth, or better, the fifth intercostal space, close to the edge of the sternum, and, in order surely to avoid wounding the heart, the operation should be performed with the patient lying on his back. We can easily avoid wounding the mammary artery. When the position of the parts is normal, it is scarcely possible to puncture the pericardium near the left edge of the sternum without opening the pleural sac at the same time, as was shown by Hammernik, and as we learn from the position of the parts observed on frozen sections of the body. But this injury of the pleural soc is of trifling importance when the capillary trocar is used with exclusion of air; 1 Lancet. Dec. 19, 1874. 624 BAUER.—DISEASES OF THE PERICARDIUM. on the other hand, we need not anticipate wounding the edge of the lung, since the latter is pressed aside by the distended pericardium. If we are considering the question of a radical operation for pyopericardium, we should first endeavor, to the best of our ability, to assure ourselves that the pericardial and costal pleune are adherent, which in long standing, purulent effu- sions, we certainly may expect to find is the case. For this reason, the advice given by Larrey and Desault, to enter between the xiphoid cartilage and the seventh left costal cartilage, though anatomically justifi- able, should not in most cases be followed, for here other difficulties are added to the operation. Whether the result of the operation is simply palliative, /. e., whether the emptied sac refills or not, would, with a larger experience, probably receive the same answer as in the operative treatment of pleuritic exudations. So far the results are favorable; that is, after the operation the emptied sac collapses, and |)ermits the lungs to expand; nevertheless a better result is attained by emptying the sac par- tially and at intervals rather than all at once. At all events, where life is threatened it is justifiable to operate, and it is also allowable to make an exploratory punc- ture with a Pravaz's s}Tringe for the purpose of ascertaining whether the exudation is purulent or not. Tubercular Pericarditis. Acute miliary tuberculosis of the pericardium is very rare, and is only seen associated with general acute miliary tuber- culosis, especially affecting the serous membranes. In the course of general acute miliary tuberculosis, the eruption on the peri- cardium is destitute of symptoms—at all events, we are not yet sure whether miliary tubercles on the pericardium give rise to friction murmurs or not, although it is quite probable they do so. Tubercular pericarditis is most frequently found in persons suffering at the same time from tuberculosis in other organs, and especially in the lungs, and either is developed from the outset in this manner, or else a simple chronic pericarditis finally assumes a tubercular form. It is rare that the latter occurs in TUBERCULAR PERICARDITIS. 625 individuals who give no evidence of tuberculosis elsewhere in the body; moreover, we must remember that, even in cases of marked pulmonary tuberculosis, a simple pericarditis is more common than the tubercular form. We may learn how rare tubercular pericarditis is even in tuberculous patients from the records of Willigk, who in one thousand three hundred and seventeen autopsies on tuberculous individuals only found the pericardium affected eleven times. Eppinger found tubercular pericarditis somewhat more frequently.1 We find in such cases a more or less abundant exudation in the pericardial sac, which is almost always markedly hemor- rhagic in character. The pericardium is in a state of chronic in- flammation, is thickened in bands, and the two coats are here and there adherent and covered with both old and recent deposits of lymph. Together with the inflammatory products, numerous gray and yellow miliary tubercles are found distributed over the serous coat, and between the bands and pseudo-membranes, and sometimes, wedged in between the muscular tissues of the heart, are seen yellow, cheesy nodules, from the size of a bean to that of a hazel-nut. The symptoms of tubercular pericarditis resemble exactly those of a simple chronic inflammation of the pericardium. In the course of the disease the watery portion of the exudation may be partially reabsorbed—a commencement of a cure, just as occurs in tubercular pericarditis. As the physical signs give no clear indication for the diagnosis of tubercular pericarditis, we can only suspect it when a chronic pericarditis occurs as a complication of tubercular disease in the lungs, peritoneum, etc. In these complicated conditions we can naturally arrive at no certain conclusion from the nature of the fever, etc. The diagnosis will be all the more uncertain from the fact that, as we have already said, even in tuberculous patients, the pericar- ditis, as a rule, has the character of a simple inflammation, and that, on the other hand, cases are unknown where the tuber- cular inflammation confined itself entirely to the pericardium. Our treatment can only be the same as that for a chronic 'Prag. Vierteljahrschrift. 1872. 113. p. 13. VOL. VI.—40 626 BAUER.—DISEASES OF THE PERICARDIUM. pericarditis—endeavoring to sustain the heart, allay the fever, and support the general health. When there is existing tubercular disease of the lung, we must avoid all depressing treatment as well as all operative procedures. The occurrence of a pericarditis of this nature will have no special influence on the treatment of the primary trouble in the lung, but it will serve to hasten the surely fatal termination of that disease. Carcinomatous Pericarditis. Carcinoma very rarely occurs in the pericardial sac, and when it does, it is as an extension of the disease from neighbor- ing parts, particularly from the mediastinum, sternum, or oesoph- agus, on to the pericardium. Much more rarely do we find nodules on the pericardium, secondary to acute miliary carci- noma in other serous membranes. Kohler found cancer of the pericardium six times in 9118 autopsies; Giinsburg once in 1700; and Willigk, in 477 autopsies on patients dying of cancer, found the pericardium affected seven times.1 When the new growth extends to the pericardium from neighboring parts, the parietal layer shows, as a rule, a diffuse infiltration of cancer, or else the mass grows from a single limited spot and projects in nodules into the sac. Associated with it, there is almost always a fluid effusion into the cavity. The fluid is frequently hemorrhagic in character, sometimes purulent and ichorous, and again in other cases it has more the appearance of serum. The symptoms may be the same as those of chronic peri- carditis or of a serous effusion. When cancer exists in the neighborhood, the development of an increased dulness over the heart, of a triangular shape, will cause us to suspect that the pericardium has become involved in the new growths, although even in such cases a simple pericarditis or a serous effusion is more common. We have alluded to the fact that under such In Duchek, loc. cit. PERICARDIAL ADHESIONS. 627 circumstances the extension of the new growth outside the peri- cardium may easily simulate enlargement of the pericardium itself as regards the signs on percussion. Sometimes when the new growth extends on to the pericar- dium we may have the signs of an acute pericarditis ; this occur- rence will also cause us to suspect cancer of the pericardium when it exists in the immediate neighborhood. Adhesions between the Heart and Pericardium, Meckel, Observ. sur les malad. du cceur. Hist, de I'acad. royale des scienc. Tom. XI. Berlin. 1875. p. 56.—Holler, Element, phys. Tom. I. Lausannae. 1757. p. 289.__ Morgagni, De sedibus et causis morb. Tom. II. lib. II. ep. 17-24.—Lieutaud, Hist. anat. med. Tom. II. lib. II. Paris. 1767.—Pohl, De pericardio cordi adher- ente ejusque motum turb. Progr. Lips. 1775.—Nebel, Progr. de pericard. cum cordo concreto. Giessen. 1778.—Senac, Traite" de la struct, du cceur. etc. Tom. II. Paris. 1783.—Corvisart, Ess. sur les mal. et les 16s. org. etc. Paris. 1818. p. Zl.—Kreysig, Die Krankh. des Herzens. II. 2. S. 623.—J! Hope, Krankh. des Herzens und der grossen Gefasse. fibers. Berlin. 1833. S. 333.—Dundas, On a peculiar disease of the heart. Med. chir. trans. Vol. I. 1815. p. 37.—Mutter, De concret. morbos. cordis cum pericard. Diss. Bonn. 1825.—Skoda und Kolletschka, Ueber Pericarditis in pathol. und diag. Beziehung. Oesterr. med. Jahrb. 28. Bd. Wien. 1839. S. 419.—Aran, Recherch. sur les adher. gen€r. du p6ricarde. Arch. gen. de med. Avr. 1844. p. 466.—Gairdner, On the favorable terminations of pericarditis, etc. Edin. Month. Jour, of Med. Sc. 1851.—Skoda, Ueber die Erscheinungen der Verwachsung des Herzens mit dem Herzbeutel. Zeitschr. der Wiener Aerzte. April, 1852. Sitzungsberichte der k. k. Akademie der Wissensch. Nov. 1851.—Kbrner, Casuistische Beitrage zur Lehre der Erscheinungen der Ver- wachsung des Herzens mit dem Herzbeutel. Wochenbl. d. Zeitschr. d. k. k. Gesell- schaft d. Aerzte zu Wien. Nos. 2 u. 5.1855.— Williams, Lectures on diseases of the chest. Deutsch von Behrend. 1841.—Francis Sipson, On the changes, etc. Worcester. 1844.—Cejka, Drei Beobachtungen. Prag. Viertelj. 1855. 2. Bd.—Law, Obs. on pericard. Dubl. Quart. Journ. of Med. Sc. Aug. 1856.—Potain, Bullet, de la soc. anat. de Paris. Aout, 1856.—Bertin, Pericard. adhes. avec caillots hemorrbg. enkyst. dans les fauss. memb. Bull, de la Soc. anat. Juil. 1857.—Traube, Zur Lehre von der Verwachsung des Herzens mit dem Herzbeutel. Med. Zeitung. hrsg. vom Vereine fiir Heilk. in Preussen. 11. 1858.—Breithaupt, Vollstandige Verwachsung des Herzbeutels mit dem Herzen. Ibid. No. 14. 1858.—Mauriac, Des adherences du pfiric. et de la ponct. de cette cavit6 sSreuse dans la pgricardite. Gaz. des Hop. 38. 1858.—Henry Kennedy, On adherent pericard., its diagnosis and its results. Edin. Med. Journ. May. 1858.—Gairdner, On the results of adherent pericard. 628 BAUER.—DISEASES OF THE PERICARDIUM. Edinb. Med. Journ. June, 1858.—Rechtseitiges pleuritisch.es Exsudat, mit Pyo- pneumothorax, Pericarditis und theilweiser Verwachsung des Pericards mit dem Herzen. Oesterreichische Zeitsch. fiir pract. Heilk. V. 41. 1859. 691.—Hinds, Does the pericard. become universally adherent to the heart after acute pericar- ditis and recov. Brit. Med. Journ. 16. March. 1861.—P. Bosisio, Not. clinich. int. ad un caso cli aderenza totale de l'peric. Ann. univers. di Med. Milano. Nov. 1861.—Skoda, Zur Diagnose der Verwachsung des Herzens mit dem Herzbeutel. Wien. allg. med. Zeitsch. 1863. 36.—Henrie-Marie Fournier, Des adherences du pericarde. These, Strassbourg. 1863.—Abelles, Deutsche Klinik. No. 31. 1859.— Geist, Klinik der Greisenkrankheit. Erlangen. 1857-60.— Oppolzer, Spitalzeitung. Nos. 10, 13, 14. 18Ql.—Jaccoud, Gaz. hebd. VIII. 1861.—Moore, Gaz. meU de Paris. 31. 1863.—Betz, Auscult. Erscheinungen bei pericard. Verwachsungen. Memorab. IV. 8. 1859, und XI. 1866.— N. Friedreich, Zur Diagnose der Herz- beutelverwachsung. Virch. Arch. 29. Bd. 1864.—E. Archer, Two spec, of extensive calc. depos. in the peric. Trans, of Path. Soc. XX. p. 191.—S. Wills, Adherent peric. as a cause of cardiac disease. Guy's hosp. rep. XVI. pp. 196-208. —E. Galvagni, Stud, clinic, Sulla sinfise card, e sul. rientram sist. Riv. clinic. di Bolog. 1873. Nov.—A. Kussmaul, Ueber schwielige Mediast. pericarditis und den paradoxen Puis. Berl. klin. Wochenschr. 37-39. 1873.—#. Cerf Die Ver- wachsung des Herzbeutels. Diss. Zurich. 1875 (contains a number of biblio- graphical references).— Webb, A case of a most extensive pericardial adh. Philadelph. Med. Times. April 15, 1872. After the erroneous supposition, that obliteration of the peri- cardial sac was a congenital defect, had been abandoned, Vieussens, Lieutaud, Morgagni, and others began to investigate the matter, both clinically and from a diagnostic point of view. Morgagni found, by the comparison of a series of forty-five cases, that the most frequent sign was absence of a visible apex beat. By various observers, as by Testa and others, severe palpitation was considered an important sign ; while Senac and likewise Cor- visart declared that irregular and tumultuous movements of the heart and the feeling of tearing in the cardiac region were essential symptoms. Heim and Kreysig asserted that they could recognize an ad- herent pericardium by a depression formed at each systole of the heart, at the left of the scrobiculum cordis, close under the false ribs. Sanders stated that he had observed an undulatory move- ment at the same place. Laennec, Bouillaud, and Piorry, however, could not satisfy themselves of the accuracy of these last statements. J. Hope described various symptoms which he PERICARDIAL ADHESIONS. 629 believed to be characteristic of adherent pericardium ; but none of these proved trustworthy. According to Williams' observa- tions, the movements of the heart can be more distinctly felt; the intercostal spaces are retracted ; the dull sound, on percussion in the pericardial region, remains the same during inspiration and expiration. All these are given presupposing a simultaneous adhesion to the anterior chest wall. Aran considers the disap- pearance of the second sound of the heart to be an essential sign. In spite of the efforts of these numerous investigators, the diagnosis of adhesions between the heart and pericardium had no solid foundation until Skoda gave us the exact information, that in a series of cases characteristic symptoms are always observed, which render a diagnosis possible. Recently Fried- reich has added another objective sign of obliteration of the pericardial sac. Etiology. Adhesions of the two pericardial layers are found varying in extent and of a more or less solid consistency. At autopsies we occasionally meet with them, either as unimportant and acci- dental conditions, or else as forming the anatomical starting-point of disease of a special character, which may lead directly to a fatal termination. We must distinguish between loose adhesions limited in character, and those which are firm and more extensive. If the adhesion is so close and so general that we can no longer recognize the point of separation of the two layers, the condition is called obsolescence or obliteration of the pericardial sac. Every adhesion of the layers of the pericardium is the product of an antecedent pericarditis. Not uncommonly the inflammation which caused the adhesion has been entirely latent, or at least has given rise to no violent symptoms. Yet abundant fibrino-serous effusions with delayed reabsorp- tion and chronic pericarditis are the most frequent causes of adhesions. In how many cases of pericarditis permanent adhe- sions remain, is, as we have already hinted, a difficult question to answer. Limited adhesions are much more frequently found 630 BAUER.—DISEASES OF THE PERICARDIUM. than those which are extensive, or those which cause total oblit- eration of the sac. Chambers found adhesions in 5 per cent, of all autopsies. Leudet saw in 1,003 autopsies adhesions in 5.7 per cent, and total obliteration in 2.5 per cent. Wil- ligk found complete adhesion sixty-eight times in 4,500 post-mortem examinations, i. e., in 1.5 per cent. According to Gairdner, extensive adhesions occur in 2.3 per cent., and slight ones in 5 per cent. more. Geist, in the examination of five hun- dred and fourteen people of advanced age (from sixty to ninety-three years), found adhesions twenty-six times—that is, in 5 per cent. Giinsburg saw it only in 1.2 per cent, of bodies examined. How far other things, besides those enumerated, serve to develop adhesions, we do not as yet know. As examples we might mention feeble movements of the heart, continued dura- tion of the inflammatory irritation, repeated renewals and cessa- tion of the inflammation, etc. Bouillaud and Ayres observed total adhesion of the pericardium in cases of new growth in the mediastinum, which had completely enclosed the heart. Barlow and Peacock saw hydatid cysts with adhesion of the pericardial layers.1 As regards age, the statements hold true which were made in reference to pericarditis. E. Cerf made a collection of forty-three fatal cases with total adhesion; and, arranged in order of age, the autopsies occurred as follows. From the 1st to 10th year............................ 3 times. " " 10th " 20th " ............................ 15 " " " 20th " 30th " ............................ 8 " " " 30th " 40th " ............................ 5 " " " 40th " 50th " ............................ 6 " '« " 50th " 60th " ............................ 3 " " 60th " 70th " ............................ 3 " The youngest of these forty-three patients was eight years old. Cases of peri- cardial obliteration occurring in early childhood have been reported also by Rilliet and Barthez, Wilks, Hope, and others. Bednar found adhesions in an infant of three months, and Billard and Hueter in new-born children. In the latter case there must have been pericarditis during fcetal life. The time required from the beginning of the inflammation, for the development of adhesions, is very different in different cases. 1 Cerf, loc. cit. PERICARDIAL ADHESIONS. 631 Sometimes the period cannot be marked at all during life, and in other cases not accurately. In one case, observed in the General Hospital jn Vienna, after eight days from the commencement of the disease, a retraction over the apex was observed with each systole, and this gradually and steadily increased; at the autopsy fresh adhe- sions were found between the apex of the heart and the pericardium.1 E. Cerf relates a case in which symptoms of adhesion were developed after nine days. Bouillaud at an autopsy saw adhesions formed in twenty-four days, which could with difficulty be torn asunder. Similar observations have many times been reported. Pathological Anatomy. The connective tissue which binds the two layers together is sometimes delicate and loose, and again firm and abundantly developed. Often, owing to the constant movements of the heart, the adhesions are drawn out into strings and fibrous cords, which possess considerable thickness and firmness; and this is especially the case at the apex. In other cases both serous layers are grown fast together. Moreover, the pericardial layers, and particularly the visceral, may be more or less thickened, so that the heart seems to be surrounded and enclosed by a firm sheath or capsule of connective tissue. Fibrous thickenings of the pericardial layers of this nature are not always present, how- ever. Sometimes we are still able carefully to separate them, and in other cases the union is so intimate that separation is impossible. Sometimes between the adhesions we find remains of the exudation imprisoned and fully encapsulated, thickened pus, and masses like pap or cream, consisting purely of chalk mole- cules, arising from calcification of the pus. Sometimes larger, irregular, brittle, chalky concretions are formed in this way. The fibrous thickenings and the connective tissue binding the two pericardial layers together may also undergo calcareous de- generation. In this way bony plates are formed, of either a rounded or an irregular, branching shape, and situated chiefly upon the visceral layer. Where the calcification is extensive, 1 Schmidt's Jahrb. Bd. 103. S. 139. 632 BAUER.—DISEASES OF THE PERICARDIUM. the heart may appear to be encased in a bony shell. In such cases it is difficult to conceive how it is possible for the heart to contract at all. Such calcifications were observed even by the older physicians. Laennec, in one case, saw the heart entirely enclosed within a bony shell. Louis, Cheselden, Gendrin, Kreysig, report similar instances. Among eighty-five cases of adhesions between the pericardial layers, Chambers observed calcific deposits five times. In a case reported by Bouillaud a concretion on the apex of the heart had perforated the pericardium. Forster and von Bamberger have also reported instances of ex- tensive calcific deposits. There was extensive calcification in the following case, a brief history of which I subjoin : S. J., set. fifty-four, a whitewashes presented himself on the 25th of May, 1875, at the Clinic of Prof, von Ziemssen. He stated that he had formerly often suffered from shortness of breath, especially upon making any physical exertion. He had never had acute rheumatism, but had probably indulged too freely in the use of alco- hol. In December, 1874, the difficulty of breathing having increased very decidedly, and the feet and abdomen having begun to swell, patient applied for admission to the hospital, and remained there under treatment six weeks, when he was discharged in an improved state of health. His condition on the 25th of May was as follows : Marked cyanosis, becoming extreme during paroxysms of coughing ; mucous membranes of a dark, livid hue; the skin of the lower extremities bluish-red and decidedly sclerotic. The external jugulars are distended with blood, and do not diminish in size even when a deep inspiration is taken; there is no visible pulsation in the veins of the neck. The eye balls are very prominent. Pulse small, soft, 104, tolerably regular, and not paradoxical. Number of respirations, twenty-four; slight dyspnoea. The apical impulse cannot be felt at any point; no murmurs ; heart sounds feeble; the second pulmonary sound alone is somewhat louder. The area of cardiac dulness does not appear to be enlarged when the patient is in the recumbent position; in the sitting posture the area of relative dulness is increased, not only in length, but also in breadth. Effusion into both pleural cavities, rather more in the left than in the right; above the effusion the respiratory murmur is vesicular at all points; loud rhonchi also audible. Abdomen large, tense; its walls cedematous; abdominal cavity contains an abundant free exudation. The left lobe of the liver seems to be exceedingly small; it extends to the linea alba near the xiphoid process; its border is hard and sharp ; the right lobe has diminished to a less extent. Owing to the presence of fluid in the left pleural cavity, the spleen cannot be accurately measured; it does not, however, extend as high up as to the arch of the ribs. Urine dark-brown; contains no albumen. Appetite good; slight constipation; almost entire sleeplessness without the aid of remedies ; dizziness ; mind acts slow- ly. Diagnosis: Degeneration of the heart muscle, connected with—in all proba- bility—old pericarditis. Died the same day. Autopsy : Body of powerful build; abdomen distended ; cyanosis; well-marked PERICARDIAL ADHESIONS. 633 dropsy. Costal cartilages ossified; both pleural cavities contain large quantities of a clear yellow serum; the lungs correspondingly compressed, in most places dry and bloodless; the bronchi very red, and their contents purulent. Pericardium adherent to heart throughout its entire circumference; anteriorly and posteriorly. but not on the sides, the connective tissue binding the two together has undergone complete ossification; marked oedema of the subserous connective tissue of the heart. On the left side, between the two layers of the pericardium, there is an encapsulated mass of substance like thick pus ; the walls of this cavity are covered with chalky scales, and the contents consist of a chalky emulsion containing no pus corpuscles. The muscular tissue of the heart is extremely thin, the left ven- tricle being to a very marked degree narrower than the right. The bundles of muscular fibres seem still to be pretty well preserved; transverse markings still distinct. A small osseous fragment, the size of a pea, rests upon the right aortic valve. The noduli Arantii are somewhat thickened; the valves, however, are apparently sufficient. Spleen, 9 x 15 ctm.; parenchyma tough, dark, and of a blackish-red hue. Liver somewhat diminished in size; nutmeg coloring ; calcific, pea-sized spots on the surface of both lobes. Abdominal cavity contains a moder- ate amount of clear yellow serum. Abundant pigmentation of the mesentery and intestinal walls. Kidneys a little increased in size, cyanotic, tough. Mucous membrane of the stomach strongly pigmented and hyperaemic. In regard to the behavior of the heart itself, after adhesions have taken place between the pericardial layers, some authors have maintained that, in addition to the complete obliteration of the pericardial sac, the organ very often undergoes hypertrophy and dilatation. The chief advocate of this view has been J. Hope, who states that he has never in a single instance failed to find these alterations. According to his view, the hypertrophy and dilatation are the necessary consequences of the adhesions, which, by furnishing increased resistance, impose additional labor on the heart. He also believed that the hypertrophy is further favored by the myocarditis which accompanies the whole process. Stokes, among others, opposes this view and, without deny- ing the possibility of such a consecutive hypertrophy, disputes both the necessity and the frequency of its occurrence. The statistics compiled by Beau and Kennedy showed that hyper- trophy is a frequent accompaniment of pericardial adhesions. Gairdner's investigations led to the opposite result. Quite re- cently Duchek, Friedreich, and others have completely refuted the idea that obliteration of the pericardial sac necessarily entails 634 BAUER.—DISEASES OF THE PERICARDIUM. a consecutive hypertrophy of the heart. This, they declare, is a common though accidental occurrence, which either existed already before the formation of the pericardial adhesions, or followed upon valvular defects coetaneously developed. It is an undoubted fact that hypertrophy and dilatation are very often wanting. The heart may be perfectly normal. This, it must be confessed, is rarely the case, and is encountered almost only in cases where the adhesions are limited in extent, or at least are not very firm. As a rule, the heart is found in a more or less well-marked condition of degeneration and atrophy. The bundles of muscular fibres show evidences of fatty degen- eration, or even of hyaline and pigment degeneration; or the appearances are those of an interstitial chronic myocarditis with its results (true cardiac stenosis, tendinous degeneration of the papillary muscles, secondary endocarditis). While in some cases these processes may, without doubt, have already begun during the acute stage of the preceding pericarditis, in others they are, as Friedreich has also remarked, the direct result of the -pericardial adhesions. Without entering into the question whether the myocarditis is the immediate result of the pericarditis, or first originates after the adhesions have taken place, the results which follow the myocarditis may be different. Thus in one case there will be simple hypertrophy and dilatation, in another degeneration and atrophy—the results, in both instances, of the myocarditis. The atrophy is clearly due to the hyperplasia of the connective tissue, and to the pressure exerted by the stiff fibrous encasement into which the pericardium becomes converted. Under these circumstances dilatation of the cavities of the heart is rendered impossible by this same rigid envelope. If the heart substance has already become flaccid and flabby before the connective tissue has acquired sufficient strength and stiffness to offer such a degree of resistance, passive dilatation of the ventricles will follow, on account of the enfeebled contracting power of the heart. The dilatation may then lead to secondary muscular hypertrophy; this will con- tinue, however, only up to the point where the cicatricial tissue begins to restrict the supply of nourishment to the heart sub- stance, and then from that time forth degeneration sets in. As PERICARDIAL ADHESIONS. 635 a matter of course, in a few cases the hypertrophy may have already been present before the adhesions formed. Adhesions may form not only between the pericardial layers, but also between the outer surface of the pericardium and the anterior thoracic wall, the pleural surface, and the organs situ- ated in the posterior mediastinal space—the oesophagus, the aorta, and the spinal column. Pathology. General Picture of the Disease. In earlier times physicians were divided in their opinions regarding the question, whether pericardial adhesions were ca- pable of exerting a disturbing influence upon the normal func- tions of the heart and upon the general health. Thus, Laennec and many others believed that obliteration of the pericardial sac was a matter of no very great importance, while Corvisart, in harmony with the views of the earlier observers—Lancisi, Mor- gagni, Vieussens and others—considered the condition as incom- patible with long life. These differences of opinion may be explained by the fact that the adhesions themselves present great differences, and consequently give rise to very different consequences as regards the functions. The pericardium may be adherent to the heart without giving rise to any disturbances whatsoever. In these cases the adhe- sions are either so limited in extent or so loose that the heart experiences no interference in its movements. At the same time the heart is neither atrophied nor degenerated, and consequently all those symptoms which usually accompany degeneration of the heart are wanting. These changes, it is true, may exist for a certain indefinite length of time with a perfect condition of health, and are only accidentally discovered, in most cases, at the autopsy, unless the observation, at some previous time, of a pericarditis, has led us to suspect the existence of adhe- sions. Of those cases in which certain functional disturbances point to the existence of heart trouble, the majority are not distin- 636 BAUER.—DISEASES OF THE PERICARDIUM. guished by symptoms that are at all characteristic or peculiar. The symptoms which are observed in enfeebled muscular con- tractility of the heart and interference with the circulation are the same as those which are wont to accompany various other affections of the heart, even chronic pericarditis. Often there is a very marked degree of cyanosis; the dis- tended veins stand out prominently upon the neck; the pulse wave is extraordinarily low, and scarcely to be felt by the finger; the pulse, too, is often irregular, the individual waves, in particular, being of different heights; the frequency of the pulse is almost always increased. The apex-beat is lost, or only a slight tremor is to be felt, and the heart sounds are usually extremely feeble. The liver is more resistant than usual, and increased in size, or, on longer duration of the process, the organ may even present the appearance of the atrophied nutmeg liver. The spleen is not unfrequently enlarged. In consequence of the diminished aortic pressure the urine is considerably diminished in quantity, of high specific gravity, high colored, and may also contain albumen. Usually the patient suffers from dyspnoea, particularly on slight bodily exertion or mental excitement, and not unfrequently also from continuous orthopnoea with praecordial distress, a ten- dency to faintness, and insomnia. The sensation of palpitation is experienced only occasionally. If death do not occur from complications, or from a sudden arrest of the heart's action, general dropsy is developed, which may attain a very high degree. Should the heart temporarily regain its energy as a result of rest, improved nutrition, the use of digitalis, etc., the secretion of urine becomes considerably in- creased, and the dropsy declines for a time, but only to return anew. In consequence of the chronic oedema of the lower limbs, scrotum and abdominal wall, the skin of these parts becomes thickened, acquires a bluish-red color, and is very apt to be attacked with erysipelas. The often copious effusions into the serous cavities add to the difficulty of respiration, and by the sensation of fulness which they occasion render the administra- tion of food more difficult. The result is invariably fatal, and may be produced by gradual exhaustion, by oedema of the lungs, PERICARDIAL ADHESIONS. 637 by hemorrhagic infarctions of these organs, or by terminal inflammations. Tliese symptoms either follow directly after the occurrence of a pericarditis, or they may develop successively without a marked beginning. The causal pericarditis may have remained latent, or it may have occurred a long time before, and have ter- minated in apparent recovery. Only a part of the symptoms mentioned are produced by the adhesions ; the rest, and in fact the greater portion, are due to the concomitant changes in the cardiac muscle, so frequently attendant upon the presence of adhesions. Even when these adhesions are of such a nature as to produce but little interfer- ence with the movements of the heart, muscular degeneration may still ensue during the further progress of the disease. Not unfrequently the functional disturbances do not make their appearance until the connective tissue of the adhesions has become more rigid, or even calcified—processes which require considerable time for their completion. The stage of muscular degeneration may be preceded by a period of hypertrophy, during which the compensatory, though probably merely incidental gain in the working force of the heart, undoubtedly better enables the organ to overcome the resistance to its contractions, produced by the pericardial adhe- sions. Cases of this kind present in their symptoms, particularly in their later stages, a great resemblance to each other,1 although they may differ very much in duration. When the cardiac movements are seriously impeded by close adhesions, symptoms ensue, which, by reason of their rare appearance, except under these conditions, are of the greatest value in the diagnosis of pericardial adhesions. These symptoms consist of an immovable position of the heart, systolic depressions of the intercostal spaces with a loss of the apex-beat, and the diastolic swelling of the cervical veins, noticed by Friedreich. Sometimes these symptoms may be observed to occur as an im- 1 Vide S. Wilks, Adherent Pericardium as a Cause of Cardiac Disease. Guy's Hosp. Report. XVI. 196-208. 638 BAUER.—DISEASES OF THE PERICARDIUM. mediate result of a pericarditis, the systolic depressions being noticed at a morning visit, whereas nothing of the kind could be detected the evening before. In such cases the derangement of the circulation, and the enfeebled action of the heart, must be produced immediately by the rapid occurrence of adhesions between the pericardial surfaces. As a rule, however, the signs referred to develop very gradually and imperceptibly, and are not detected until after complete adhesion has taken place. The firm adhesions, which are the subject of present con- sideration, are scarcely ever broken up, and always prove fatal after a period varying with the firmness of the agglutinations and the progress of the muscular degeneration. The reported cases, in which the supposed signs of adhesions disappeared again, were presumably instances where the connections were so slight as to be ruptured when the heart recovered its energy. The rapid disappearance of pericardial friction sounds during the course of pericarditis is by itself not to be regarded as an indication that adhesion has taken place, because the same sudden disappearance may be produced by several other causes. On the other hand, the friction may still continue to be audible for some time after the surfaces have become partially adherent. Analysis of Individual Symntoms. To describe more fully the subjective and objective symptoms occasioned by the derangement of the circulation, would be merely to repeat what is already obvious, viz., that they constitute the most striking part of the symptoms of pericardial adhesions. For historical reasons, however, the sensation of palpitation requires special mention, because several of the earlier observers, Vieus- sens, Lancisi, Lower, Baillie, Testa and others, have laid great stress upon this symptom. Palpitations, however, occur only in a minority of cases, and present no characteristic features. When they are present to a noticeable degree, it is usually in connec- tion with hypertrophy of the heart. The different views, which still prevail up to the present time, in regard to the occurrence of hypertrophy of the heart as a re- sult of pericardial adhesions, and in regard to the way in which PERICARDIAL ADHESIONS. 639 this result is produced, have been already considered in the dis- cussion of the anatomical conditions. The differences of opinion in regard to the relative frequency with which cardiac hypertrophy is encountered will be reconciled, if we avoid starting out with generalizing views of the significance and genesis of the lesion. If hypertrophy be met with in some cases, and atrophy in others, it is evident, without determining the exact relative fre- quency of these opposite events, that the pericardial adhesion is not necessarily followed by hypertrophy, and that the opposite result, the atrophy, which is found in so many cases, must be produced by the presence of some other factor. If we examine the anatomical descriptions of the cases where marked atrophy existed, we find very frequently that special mention is made of the firmness of the adhesions, and of the presence of calcifica- tions ; and it is only fair to suppose, therefore, that the nature of the adhesions must have some influence upon the occurrence of this lesion. It is the pressure of the cicatricial tissue upon the nutrient vessels, and upon the muscular substance itself, which initiates the atrophy, while the passive dilatation of the cavities is prevented by the resistance of the enveloping capsule. Whether the traction of the cicatricial tissue may not in many cases also operate excentrically, and thus bring about a dilatation of the ventricles, especially when the parts are fastened to the spinal column or the anterior chest wall, I shall not venture to decide. While we must concede that such an event is possible, it is certainly rare. In the opinion of Hope and his followers, it is the increased resistance to the cardiac movements which calls forth a com- pensatory hypertrophy. But, unfortunately for this view, it is just in the cases where the adhesions are the firmest, and the resistance the greatest, that hypertrophy fails to occur. Fur- thermore, if we admit that the serious impairment in the nutri- tion of the muscle in these cases tends to prevent the occurrence of hypertrophy, it follows equally that the view, according to which the work of the heart is increased by the adhesions, must be erroneous, and that, instead of adding to the normal work, the lesion actually diminishes the capacity of the heart for its usual task. 640 BAUER.—DISEASES OF THE PERICARDIUM. Only in those cases where a passive dilatation of the ventricles has occurred early in the disease, before the connective tissue has exerted its concentric traction, can there have been any occasion for the performance of increased work, and in such instances hypertrophy may result, if the conditions of nutrition are favor- able. If it were demonstrated that a concentric hypertrophy of the heart does take place in cases of obliteration of the pericardial cavity, this fact would militate against the view expressed above. I have never, however, seen a case of this kind, nor do I think that even such a condition ought to be ascribed to a muscular hyper- trophy induced by the additional work made necessary by adhesions. Cardiac hypertrophy from this cause is brought about in just the same way as the muscular hypertrophy resulting from idio- pathic myocarditis. In both cases the lesion may affect the entire organ or only one of its divisions. In the further course of such cases, too, there prevails a similarity in many respects to hypertrophy of the heart as it occurs without pericardial adhesions. In consequence of the pressure of the tissue which constitutes the adhesion, a degenera- tive stage, with all the symptoms proper thereto, may occur within a comparatively short time. Under this head belong relative valvular insufficiencies. Cases of the sort are described by Jaccoud, Schiitzenberger, Marvaud, and others. We then observe valvular murmurs, and, in insufficiency of the tricuspid, marked venous pulsation, etc. The hypertrophy of the heart, whether produced in this way or already present before the formation of the adhesions, may give rise in many cases to a plainly perceptible apex-beat in spite of the adhesions present, whilst otherwise the apex-beat is wanting, or only a feeble tremor is to be felt. In forty-five cases of obliteration of the pericardial sac Morgagni observed absence of the apex-beat thirty times. Moreover, in obliterations of the pericardium absence of the apex-beat may depend solely upon feebleness of the heart's action, the adhesions not being firm enough to hinder the corresponding change in the heart's position. Such being the case, an apex-beat may at times be perceptible and at other times not. So soon, however, as the adhesions acquire a very PERICARDIAL ADHESIONS. 641 firm character, they may so hamper the mobility of the heart as to render the systolic sinking and erection of the organ impossi- ble. Very commonly both causes—weakness of the heart's action by reason of an affection of the muscular tissue, and the hindrance due to adhesions—work together. Skoda observed a systolic beat in the region of the base of the heart, and in one case a sort of pulse-beat in a partial aneurism of the heart. If the pericardium be adherent to the anterior thoracic wall over a considerable area, the apex-beat, if there be one present, must necessarily remain unchangeable as regards its locality in all postures of the body. Inasmuch as this fixation hinders the downward movement of the diaphragm, the inspiratory bulging below the ribs may appear less on the left side than on the right. According to Williams, who first insisted upon these relations, we feel, in adhesions of this sort, the same close contact of the heart with the anterior chest-wall on both inspiration and expiration. Williams has pointed out also that in adhesions of the pericardium to the anterior wall of the chest, if at the same time the borders of the lungs be adherent, the absolute cardiac dulness will remain unchanged on inspiration and expiration. Frequently, too, in this condition of things we find the absolute cardiac dulness somewhat enlarged, according to the retraction of the borders of the lungs as a result of the fixation. If, however, adhesions of the pericardium exist without accom- panying adhesion to the anterior chest-wall, and without fixation of the pulmonary borders, the absolute cardiac dulness will, as a matter of course, be diminished in extent during inspiration. Hence, we should draw no further conclusion from unalterability of the absolute cardiac dulness than what this symptom strictly proves. It is only in connection with other data that tliese extrapericardial adhesions are of value in the diagnosis of oblit- eration of the pericardial sac. The most important phenomenon in adhesions of the pericar- dial layers consists of a systolic depression in the place of the deficient apex-beat. Besides the systolic depression at the locality proper to the apex-beat, pittings may also be present in two or three intercostal spaces to the left of the sternum. VOL. VI.—41 642 BAUER.—DISEASES OF THE PERICARDIUM. Systolic depressions in one or more intercostal spaces to the left of the sternum, while at the same time the apex-beat is present, are observed under various circum- stances, without the pericardial layers being adherent. Diverse views have been advanced as to the causes to which these systolic depressions are to be attributed. Under normal conditions they do not occur, because the heart, in its systole, presses with a uniform surface against the front wall of the chest, and because the vacuity thus produced is filled out by systolic distention of the lungs. If these normal conditions are abolished, from any cause, the intercostal spaces must sink in during systole. See the introduction to this volume. According to Skoda's original idea, which most physicians have followed, the above-described systolic pittings can occur only when the pericardium is adherent at one and the same time to both the heart and the anterior chest-wall. But, in the first place, Traube has shown by a case that a single band of connec- tive tissue between the heart and the pericardium may give rise to systolic indentation in the region of the heart's apex, and that an adhesion between the mediastinal and the costal pleura is in no wise necessary to its production. Traube afterwards observed a case in which, in spite of systolic pitting, there was no adhesion between the heart and the pericardium. Instead of this, an exceptionally tense fold was found along the posterior wall of the pericardium, which, arising near the opening for the emergence of the pulmonary artery, and extending downwards, was inserted into the left wall of the auricle, and could be traced along this nearly to the sulcus transversus. This anomalous duplicature was capable of hindering the systolic movement of the base of the heart forwards, downwards, and to the left. Since then further observations by Baler, and especially by Friedreich, have proved that systolic pitting at the site of the apex-beat may occur without any adhesion of the heart to the pericardium. Friedreich saw the most palpable systolic pitting at the site of the apex-beat in a patient with well-marked stenosis of the aorta and left lateral hypertrophy, but at the autopsy the pericardium was shown not to be adherent. Friedreich's explanation of the occurrence of systolic pitting in the last-mentioned case was that the heart, in consequence of deficient backward impulse from insufficient filling of the aorta, could not perform the normal motion. This explanation seems to be perfectly correct for this case, and upon the strength of it PERICARDIAL ADHESIONS. 643 we may state in general terms that systolic pitting at the site of the apex-beat may be present in all cases in which the normal movement of the heart downwards and to the left, with elevation of the apex, is hindered, provided at the same time the lungs do not sufficiently approach each other, and the contraction of the heart is powerful enough to force the apex away from the chest-wall. Under such circumstances the pitting follows, as a matter of course, from atmospheric pressure. Plainly, the causes which have just been mentioned as hin- dering the motion of the heart are found most frequently, but by no means exclusively, in cases of pericardial adhesions. Hence the resulting systolic pitting cannot be taken as absolute proof of the existence of pericardial adhesions. The systolic movement of the lungs is doubtless capable of hindering the sink- ing-in of the intercostal spaces ; but it seems to me doubtful if the borders of the lungs need be fixed in order for the occurrence of depression by atmospheric pres- sure. I am much more certain that the systolic movement of the lungs may be hindered by other causes. Furthermore, I am unable to decide as to how far the resisting capacity of the intercostal muscles is to be taken into account. We may imagine that the resist- ances to the systolic movement of the lungs are in no wise absolute. Such being the case, may it be that systolic pitting occurs in weak, emaciated persons, and not in those possessed of muscular strength ? Apart from the influence of atmospheric pressure, if the heart be perfectly fixed and its contraction powerful, the sys- tolic contraction of the cardiac muscle may give rise to pitting of the intercostal spaces. If, indeed, the pericardium be adherent both to the anterior chest-wall and to the vertebrae, the fixation of the heart will be so complete that its contraction must, almost of necessity, cause sinking of the intercostal spaces. It is precisely under such circumstances that systolic pitting is most commonly found, not only at the site of the apex-beat, but more widely diffused, combined at the same time with systolic retrac- tion of the lower costal cartilages and of the lower part of the sternum. Thus far there is no case known in which such forcible retraction has occurred in any other way than as the result of pericardial adhesions. Hence its presence must be held as con- 644 BAUER.—DISEASES OF THE PERICARDIUM. elusive in diagnosis. On the other hand, it is not absolutely necessary to the production of this forcible and diffused retrac- tion that the pericardium should be fixed to both the anterior chest-wall and the vertebral column. Thus, Friedreich has observed marked systolic retraction of the cardiac region, the ribs, and the sternum without the existence of any such external adhesions of the pericardium. Friedreich assumes, on the contrary, that it is essential to the production of this pitting that the lower surface of the heart should be firmly adherent to the diaphragm, so that the heart in contracting must draw the diaphragm upwards and its point of attachment to the chest-wall inwards. In this wise, too, according to Fried- reich, may we explain the fact that this pitting is more marked and more noticeable at the height of the inspiration, whilst the descent of the diaphragm operates in opposition to the heart, so that the latter, in order that its apex may execute an equally great movement upwards, must draw the chest-wall still more forcibly inwards, since at this moment the connecting band is shortened. There are many considerations which make against this explanation of Friedreich's.1 It may be avoided, too, without doing violence to the facts, if we remember that the natural attachments of the pericardium are of themselves sufficient to occasion pitting of the cardiac region, provided the base of the heart be fixed immovably in the pericardium. Moreover, we must take into account the action of atmospheric pressure. We may see often enough, indeed, how in patients with emphysema the lower portion of the chest-wall is pressed in on inspiration. If the heart is to draw the intercostal spaces inwards by its diminution in size, its contractions must take place with a certain amount of force. It is therefore on account of impaired 11 will simply mention here that it is not yet by any means certain that the apex of the heart makes such an extensive upward movement as to stretch that portion of the diaphragm in question, out of proportion to its mobility and capacity for yielding, and thus depress its point of insertion. Furthermore, I do not believe that the fixed portion of the diaphragm can contract in such manner that the inspiratory intensifica- tion of the phenomenon can be explained by the force of the same. In point of fact, it must be referred to atmospheric pressure. PERICARDIAL ADHESIONS. 645 cardiac force that in many cases we see this marked retraction disappear after a time. In like manner may we explain Skoda's failure to find pitting in cases of simultaneous fixation of the pericardium to the vertebral column, the anterior chest-wall and the diaphragm. If the heart's power be sufficient, pitting may occur in spite of these manifold adhesions. According to von Dusch, the pitting does not exactly corre- spond with the beginning of the systole in point of time, but is synchronous with the radial pulse, and is thus noted somewhat later than the carotid pulse. Together with sj^stolic pitting, a diastolic concussion from the apex may occur, if the apex during diastole sinks down again upon the chest-wall. This phenomenon is designated as diastolic heart-beat. In those cases in which the lower portion of the chest-wall is forcibly incurvated, the latter flies back into its original position with a jerk or shock. It is by means of its own elasticity that the chest-wall suddenly resumes its proper contour as soon as the overpowering force ceases, with the beginning of the diastole, to act. The diffuse impulse thus produced may be very plainly felt by the applied hand. According to Friedreich, the rebound of the chest-wall produces a dull sound, which may be heard on auscultation after the second sound of the heart. In this way the second sound seems split or doubled. Just this sort of doubling of the diastolic sound is frequently observed in obliteration of the pericardium. This phenomenon is therefore partly explained by vibrations of the thorax ; but, if none such are present, and yet a division of the diastolic sound is heard, it is due probably to a lack of synchronism in the closure of the pulmonic and aortic valves (Skoda), which indeed is not rare under other circumstances. Friedreich has described also peculiar phenomena pertaining to the cervical veins, which likewise are connected with the sys- tolic retractions and are never present in a striking degree without them. These include, according to Friedreich, a sudden diastolic collapse, or subsidence of the cervical veins {often tensely filled during systole), so that they disappear from view. Even the supra-clavicular fossae may become deepened at the same time. This subsidence takes place in entire synchronism with the dias- 646 BAUER.—DISEASES OF THE PERICARDIUM. tolic beat against the chest-wall, and alternates with the carotid pulse. In a case contributed by von Dusch, decided dicrotism was perceptible together with this phenomenon, whilst the first sud- den collapse was followed by a second and more complete one. Friedreich has explained the phenomenon observed by him, and which cannot very well be confounded with a venous pulse, by the hindrance offered to the return of blood through the cer- vical veins by the diminution of the thoracic space during systole, whilst the sudden diastolic enlargement of the same must have an aspiratory effect. It is probable, too, that under the given conditions the diastole must take place more forcibly and quickly on account of the traction of the adhesions from without, and the descent of the raised diaphragm. Friedreich also assumes, that, in consequence of the diastolic descent of the heart, especi- ally as caused by the action of the diaphragm, the large vascular trunks, including the superior vena cava, undergo an elongation, by means of which the downward current of blood from the cer- vical veins is likewise hastened. The dicrotism observed by von Dusch is probably to be referred to the diastole of the auricle and ventricle. Diagnosis. In the majority of cases of pericardial adhesions, great diffi- culties stand in the way of a sure diagnosis ; in fact, it is quite often impossible to make the diagnosis. This is true, not only of those cases in which there is an entire absence of symptoms, but also in those in which it is impossible to decide whether the symptoms are due to a degeneration of the heart muscle alone, or to this condition in conjunction with pericardial adhesions. If the area of cardiac dulness is enlarged, if the borders of the lungs are bound down by adhesions, the case may be one of chronic pericarditis. In the latter case, variations are observed at times in the area of cardiac dulness, corresponding with the variations in the amount of the exudation. In distinguishing pericardial adhesions from a primary degen- eration of the heart muscle, material assistance may be obtained PERICARDIAL ADHESIONS. 647 by looking carefully into the previous history of the oase, for the purpose of ascertaining whether the patient has or has not had a pericarditis. I do not agree with S. Wilks in the view that in individuals of mature age, where severe heart symptoms are present, without valvular murmurs, we may infer the existence of degeneration of the heart muscle, but that in youthful indi- viduals the same state of things points rather to pericardial adhesions ; my own observations show that also in youthful indi- viduals degeneration of the heart muscle is more common than pericardial adhesions. Among the objective symptoms, we can place no safe reliance upon the size and shape of the area of cardiac dulness, for in obliterations of the pericardial sac this area may be normal, or it may be either larger or smaller than normal. On the other hand, we may consider it a valuable sign if the area of cardiac dulness remain unchanged in size and shape. Absence of the apex-beat is not of very great value in differential diagnosis. I cannot admit, however, that under certain circumstances, the movements of the heart, which are felt by the hand when placed upon the chest, present, in pericardial adhesions, certain charac- teristics which are not observed in every case of hypertrophy of the heart—provided, of course, that there are no systolic re- tractions. The character of the pulse also presents no distinctive features to aid us in the diagnosis. We are, therefore, often compelled to refer the disturbance in the circulation to some disease of the heart without valvular de- fects, and to leave undetermined the question of the existence or non-existence of pericardial adhesions or disease of the heart muscle. If a valvular defect is associated with pericardial adhesions, the difficulty of making the diagnosis is greatly increased, for the thought of an uncompensated valvular defect is very apt to divert the mind altogether from the idea of pericardial adhe- sions. A tolerably sure diagnosis can only be made in those quite rare cases in which well-marked systolic retractions and Fried- reich's sign are present. On the other hand, the rarity of these 648 BAUER.—DISEASES OF THE PERICARDIUM. cases is still further increased by the fact, that the progressive degeneration of the heart muscle soon causes these manifesta- tions to disappear. Course and Prognosis. It has already been stated, that in a certain number of cases pericardial adhesions do not constitute a very serious affection, for the reason that they do not interfere in any way with the normal functions or with the continuance of life. In those cases in which functional disturbances manifest themselves, the course of the disease is not a rapid one, but extends over a period of months, or even years. The fatal termination occurs earlier or later according to the progress of the changes in the heart muscle and the nature of the adhesions. The result also depends in a measure upon individual circumstances and upon certain complications that may arise. If the symptoms of failing heart-power are pronounced, it must not be forgotten that, under favorable circumstances, the disturbances in the circulation may still be rectified, and the existing dropsy absorbed; as a rule, however, this improve- ment is not of long duration. The most unfavorable cases are those in which the disease of the heart muscle makes rapid advances, or those in which pro- gressive atrophy of the heart renders the organ less and less capable of maintaining the circulation. On the other hand, if the heart muscle remains in a sound condition, the existing obstacles will, in the majority of instances, be overcome by compensation. This is especially true of those cases in which hypertrophy of the heart exists at the same time. So far, therefore, as the prognosis is concerned, a strong action of the heart, and a well-marked systolic retraction of the chest-wall (provided at the same time well-marked indications of stasis are absent), are relatively favorable indications, at least for the near future. If there are reasons for believing that the heart muscle is undergoing progressive degeneration, we may then predict the probable occurrence of death within a few weeks or months. INDURATED MEDIASTIN0-PERICARD1TIS. 649 Under all circumstances we should consider every case of peri- cardial adhesions which is capable of calling into existence any symptoms whatever, as constituting a serious disease of the heart, which can, in a direct manner, lead to death at the end of a shorter or longer period of time. Treatment. Treatment can exert no influence upon the adhesions them- selves. The attempt to loosen them by exciting violent action of the heart, would certainly be in vain when they were composed of firm connective tissues, and, on account of the accompanying danger, would also be impracticable when they were recent. The degeneration of the muscular tissue must be considered as the most important element. Consequently the treatment must be mainly directed with a view to this. The presence of adhesions does not change the principles which underlie the treatment of simple myodegeneration. The results of strengthen- ing treatment addressed to the heart, together with rest and suitable nourishment, are very significant in many such cases. Especially does the proper and carefully watched use of digi- talis correct for a time the disturbance of the circulation. When dropsy coexists, the use of digitalis may be associated with diuretic remedies and diaphoretic measures. Puncture may be necessary to remove large serous effusions from the abdominal or pleural cavities. Subjective troubles, loss of sleep, require narcotics. Most active stimulation must be employed if symptoms of collapse appear. Indurated Mediastino-pericarditis and Paradoxical Pulse. At the Tubingen clinic in 1854, Griesinger1 observed a case in which the autopsy showed fibrinous mediastinitis together with fibrino-purulent pericarditis. Stiff stringy exudations were found in the connective tissue in which the large ves- 1 Beitrag zur Diagnose der Mediastinitis, by A. Widenmann, Diss, inaug. Tubingen. 1850. 650 BAUER.—DISEASES OF THE PERICARDIUM. sels are imbedded after their exit from the pericardium. Some of the venous trunks were notably constricted, as was also the aorta in its ascending portion and arch ; it was also indented and partly twisted about its axis. The pericardial cavity was almost obliterated by fibrinous membranes. At one point only was there found a circumscribed, encapsulated collection of pus. The anterior surface of the thick- ened pericardium was also covered with membranes. The heart was pale, shrunken, and flabby. The patient was a young man who had previously been healthy; the affection was probably of traumatic origin and caused death in about nine weeks. It began with stitch in the side, dyspnoea, bloody sputa, followed by cyanosis and general dropsy. Examination of the heart showed only a slight enlargement of the area of dulness, weak apex-beat, and muffled sounds. A small irregular pulse was noticed in this case during life, while the heart beat regularly. Griesinger noticed also that the intermission of the pulse occurred at regular intervals and simultaneously with inspiration.1 This observation of Griesinger's entirely escaped general notice until Kussmaul brought it to light in 1873. Kussmaul observed two similar cases in which this affection was suspected, principally on account of the character of the pulse, the pulsus inspiration inter- mittens, or pulsus paradoxus. Kussmaul selected the name indurated mediastino- pericarditis for this affection which Gendrin has described less distinctively as fibropericarditis. (See page 569.) Fig. 6. Kussmaul's pulsus paradoxus. 1st Case. Kussmaul's first case2 was that of a youth twenty-one years old, previously healthy, who fell ill the latter part of October, 1872, with indefinite symptoms and without known cause. A sense of constriction and pain in the side then appeared and the patient took to his bed. On the 18th of December the physician found pleurisy on the left side, with fever, sweats, loss of appetite, cough with watery mucous sputa, which on one occasion contained streaks of blood. In January, 1873, the pleural exudation decreased steadily, but fche dyspnoea continued, the pulse remained small, frequent and irregular, and dropsy appeared. While the case was under observation in Kussmaul's clinic the temperature at the beginning (from the 1st to the 26th April) was always below the normal, the pulse 1 Vierordt, Die Lehre vom Arterienpuls. Braunschweig. 1855. Taf. II. der Curv. N. XXV. 2 Ueber schwielige Mediastino-Pericarditis und den paradoxen Puis. Berl. Klin. Wochenschr. 1873. No. 37 et seq. INDURATED MEDIASTIXO-PERICARDITIS. 651 never less than 100, usually from 100 to 120, small and intermitting; it disappeared with inspiration and returned with expiration. After every second beat and perhaps an incomplete third, it intermitted. The respiration was quickened, the apex-beat could not be felt. The area of pericardial dulness extended upward to the third intercostal space, passed one and a half centimetres beyond the right border of the sternum, and extended on the left nearly to the mammary line. The heart sounds were uncomplicated, muffled, and weak; their rhythm was regular, notwithstanding the intermissions of the pulse in the arteries. The boundaries of the heart altered considerably with deep inspiration, especially on the left. The veins in the neck, especially the right internal jugular, were greatly distended. The liver was swollen, the appetite small, urine scanty and reddish-yellow, with traces of bile and albumen. Fig. 7. Kussmaul's pulsus paradoxus. 1st Case. Later, in the course of the disease, the temperature often rose above the normal. On the 20th of May paracentesis of the abdomen was performed and six litres of liquid removed. By the first of June the dropsy had again become very great. The jugular veins were considerably swollen, that on the right side undulated. Their distention was slightly increased with each inspiration. Puncture was repeated on the 10th of June, and on the 17th the skin of the right leg was incised to relieve the oedema. Phlegmonous inflammation set in about the incision and caused death on the 22d of June. The disease had lasted about eight months. At the autopsy the right lung was found attached about its root by a number of tough fibres to the pericardium and the mediastinum above it. On the left the tongue-shaped lobe was attached by stout adhesions to the pericardium and dia- phragm ; the upper lobe also was closely adherent to the posterior surface of the pericardium up to the point where the large vessels are given off. In front, the pericardium was free over the region corresponding to the conus arteriosus and the limits of the left ventricle. All the rest of it was attached by strong connective tissue to the diaphragm, lungs, and anterior wall of the chest. Above the peri- cardium the two layers of the mediastinum formed a normally constituted mem- brane. The fibrous layer of the pericardium was thickened and firmly attached to the visceral layer by a recent tough fibrous membrane. At the point of origin of the large vessels the fibrous pericardium increased in thickness. Tough bands of connective tissue, enclosing the remains of crumbling masses of fibrin, extended from the base of the heart into the cavum mediastini and accompanied the large vessels upward. These indurated bands formed loops about the arch of the aorta and the ascending portion. The arch of the aorta was 652 BAUER.—DISEASES OF THE PERICARDIUM. thereby drawn downwards and somewhat bent at the origin of the innominata; the ascending portion of the aorta was compressed from before backwards, so that it would scarcely admit the little finger. The trunk of the arteria pulmonalis also was compressed. Kussmaul's second case was a woman thirty-two years old, who had suffered for years with chronic bronchitis and chronic pneumonia. The time when the medias- tino pericarditis began was not determined. When brought to Kussmaul's clinic, in the latter part of June, 1873, she presented general dropsy, cyanosis, dyspnoea, with orthopncea at times. The urine contained no albumen and was diminished in quantity. While the heart's action continusd regularly, the pulse became smaller or imper- ceptible with every inspiration, and returned to its original fulness during expira- tion. The wave was small, the tension slight, the frequency from 104 to 140 The inspiratory intermission occurred in all the arteries that were accessible. There was Fig. 8. Kussmaul's pulsus paradoxus. Second Case. also a slight increase in the area of precordial dulness, absence of apex-beat, weak, muffled heart sounds, consolidation of the left lung. Respiration was frequent, dyspnoic, the supra-clavicular fossae distended by the bulbs of the internal jugulars, the external jugulars also distended. The patient's temperature was usually sub-normal in the morning, normal or somewhat raised in the evening. The dyspnoea and dropsy steadily increased, and death took place on the 20th of July. At the autopsy the pericardium was found immovably attached by strong ad- hesions ; only a small part of the right ventricle on the left and in front was free. The thick adhesions extended to both lungs, the anterior wall of the thorax, the diaphragm, and the lower dorsal vertebrae. The pericardium, and principally its fibrous layer, was so thickened that it could not be thrown into folds. The visceral layer also was thickened and condensed. The serous surfaces were covered with crumbling false membranes, composed of fibrin and connective tissue, and were glued together. From the point of reflection of the pericardium at the base of the heart, thick, indurated cords extended into the cava mediastini anticum and posticum, and accompanied the large vessels, constricting and shortening them by traction. Tough cords stretched especially from the base of the left ventricle forwards over the pulmonary artery, back to the arch of the aorta, which they indented slightly in several places and drew directly downwards towards the compressed arteria pul- monalis and the left ventricle. The valves of the heart presented no important lesions ; the muscular tissue was pale and soft. INDURATED MEDIASTINO-PERICARDITIS. 653 In a third case which Kussmaul observed during life the symptoms were iden- tical. The pulse, frequent and small, intermitted at every deep inspiration. Both internal jugulars and the superficial veins of the neck were enormously distended, but neither undulated nor pulsated. At every forced inspiration the bulbs of the jugulars became greatly swollen, and subsided again during expiration. F. Kipp' recorded a case in which the diagnosis of mediastino-pericarditis was based upon a paradoxical pulse. The case differed, however, essentially from the preceding one in this, that the formation of the indurated cords had not taken place upwards along the great vessels. Cases of the kind are less rare. The same was seen in the garrison hospital at Berlin. The patient was a young man previously healthy, and it was probable that a pleurisy several years before had been the beginning and foundation of the subsequent chronic mediastino-peri- carditis. While he was under observation, from the 3d of October until his death on the 16th of November, the important symptoms—cyanosis, dyspnoea, and general dropsy—were present. The area of precordial dulness was increased, and extended upwards to the third rib; the heart sounds were uncomplicated and moderately loud; the apex-beat could not be felt. The area of dulness did not change during deep inspiration. The jugulars were distended, and there was an indication of a venous pulse. The pulse intermitted completely at every deep inspiration. The urine contained no albumen ; its quantity was diminished. At the autopsy the sternum was found more firmly fastened down than usual by tense connective tissue of new formation. After its removal a membrane became visible which corresponded in shape to the area of dulness of the heart. Encapsu- lated, cheesy masses were found under the left costal cartilages. The boundary between the lungs and mediastinum could not be made out. The diaphragm was ad- herent to the pericardium to an unusual extent, and greatly hypertrophied. The in- durations, enclosing cheesy masses, extended to the left over the lower lobe of the lung as far as the axillary line ; the right lung was tightly adherent only at its lower part to the pericardium. The pericardial cavity was entirely obliterated; the entire ventricular portion of the heart was imbedded in a stiff callosity. The heart was considerably dilated and hypertrophied; the valves normal. The formation of the callosities had not extended far above the ventricles. The vessels leading to and from the heart were dilated. Their inner surface was polished everywhere. Connective- tissue bands, capable of drawing the vessels forward and causing indentations in them, were not found. The muscular tissue showed commencing fatty degen- eration. The symptoms, as they appear in the above described cases, agree essentially with those of chronic pericarditis or obliteration of the cavity of the pericardium. The intermitting pulse was peculiar to them. Since Kussmaul's publication it has been shown that this phenomenon is not the exclusive criterion of mediastinitis fibrosa. With reference to diagnosis, the symptom observed in the veins of the neck by 1 Ein Fall von schwieliger Mediastino-pericarditis. Dissert, inaug. prass. v. Ziems- sen. Munchen. 1875. 654 BAUER.—DISEASES OF THE PERICARDIUM. Kussmaul is a more exact indication of the presence of an indurated mediastinitis. The traction of the indurated bands during forced inspiration produces a visible, or even a considerable distention of the veins of the neck instead of the normal reduction. Kussmaul considered the occurrence of the paradoxical pulse in these cases de- pendent upon the fact, that the indurated cords encircled the aorta and drew upon it. According to his observations it is not necessary that the trunks of the vessels should be immediately adherent to the sternum (Griesinger). It is sufficient if the callosities extend from the pericardium to the large vessels, for the former is drawn forwards during inspiration, and thus traction is exerted. Fig. 9. Pulsus inspiratione intermittens, according to Baeumler. There are observations by Traube * and almost simultaneously by Baeumler,2 from which it appears that the cause of the paradoxical pulse ought not to be sought exclusively in the formation of indurated bands in the mediastinum. Both observers saw the phenomenon in question occur in pericarditis exsudativa without mediastini- tis. These cases differ from Kussmaul's in this, that the symptoms in the veins of the neck were absent, and the heart sounds became weaker during inspiration. Traube thought he found a substantial explanation in an accompanying notable thickening of the pericardium, because the tension of the stiff pericardium produced by the diaphragm during inspiration would interfere with the contraction of the Ventricles, especially if the heart were weak. Fig. 10. Pulsus inspiratione intermittens, according to Traube. The explanation given by Traube will not do for all cases, at any rate. The stiff- ness of the pericardium upon which it depends was not present in Baeumler's case, and the thickening was not considerable in the following case from von Ziemssen's clinic: 1 Berl. Klin. Wochenschr. 1874. No. 21.-Charite-Annalen. 1876. S. 270. 2 Deutsch. Archiv fur klin. Med. Bd. XD7. INDURATED MEDIASTINO-PERICARDITIS. 655 Anna E., sixty years old, could remember no previous diseases; a fortnight before admission she was taken with difficulty in breathing, tormenting cough, and pain in the left side. Frequent, dyspnoic respiration ; on making slight exertion the number of respi- rations doubles; frequent orthopnoea. The internal jugulars are dilated on both sides and pulsating. The veins of the neck do not become greatly distended during inspiration. The pulse very rapid, its volume small, not tense, perfectly regular during expiration and the following pause; as inspiration begins the pulse sinks to a minimum, and if the inspiration is deep it becomes imperceptible. The apex-beat can be felt distinctly nowhere, but when the breath is held a diffused jarring can be perceived. The area of precordial dulness is considerably enlarged ; it reaches, when the patient is lying down, to the attachment of the second rib, and when she is sitting up, somewhat higher, and is lost on both sides in the dulness due to the bilateral pleural effusion. The heart sounds are uncomplicated, muffled, and weak, are not noticeably changed during inspiration; the second pulmonary sound is some- what louder. Furthermore, there is consolidation at the apices of the lungs, especially on the left side; the resistance of the liver is increased, the anterior border of the spleen is two centimetres from the curve of the ribs, the urine is very scanty, with brick-dust 9ediment, and without albumen. General dropsy, considerable cyanosis, temperature at times slightly raised. During the whole period of observation, from the 15th of May to the 1st of July, the pulse remained paradoxical. At the autopsy a considerable effusion of hfemorrhagic liquid was found in both pleural cavities, the lower portions of the lungs were without adhesions, were greatly compressed on both sides, especially the left, and there were several hsemorrhagic infarcti in the right lower lobe. There was a large amount of haemorrhagic liquid in the cavity of the pericardium, both serous surfaces were covered with fibrinous layers, especially where reflected at the origin of the large vessels. There were also partial adhesions of the heart to the pericardium at the lower portions, firm at the point, loose on the sides. The pericardium was thickened, exclusive of the fibrinous coating. The cavity of the right ventricle small, the muscle thin, the layer of fat thicker than the muscle. The left ventricle likewise diminished, its muscle thin, pale, and brittle ; on examination with the microscope it showed marked pigment- degeneration. All the valves normal. No inflammation on the outer surface of the pericardium, nor in the mediastinum. To these cases of pericarditis exsudativa may properly be added an observation by W. Graeffner.1 In a patient with purulent pericarditis and double pneumonia the pulsation in all the arteries that could be felt became less during inspiration. If the thorax was maintained for some time in the position of inspiration the pulse remained uniformly small, and the converse took place when the expiration was prolonged. Weakening of the heart sounds and swelling of the veins of the neck Were not perceptible during inspiration. 1 Berl. klin. Wochenschr. 1876. No. 27. S. 386. 656 BAUER.—DISEASES OF THE PERICARDIUM. Fig. 11. Fig. 12. After the removal of the sternum at the autopsy the pericardium was found entirely free. The edges of the lungs touched each other nowhere, and were ad- herent to the pericardial pleura on both sides at the points corresponding to the ends of the costal cartilages. The pericardial sac contained about three hundred grammes of purulent exudation. Both layers of the pericardium were covered with a thick tufted coating, as were also the aorta and pulmonary artery, the former only to the point where it turned. The aorta was also bound down by circular adhesions which, short and tense, ran over it from the pericardium. Graeffner considers the paradoxical pulse in this case the result of the firm attachment of the pericardium to the pleura on each side, by which the inspiratory traction upon the pericardium was transmitted to the bands encircling the aorta and exerting their tension from the point where it turned to the inner surface of the parietal layer. The consequence was indentation of the vessel and diminution of its lumen. I add further that one of our colleagues shows this peculiarity of the pulse exquisitely. His radial pulse, which is perfectly normal, disappears completely at every deep inspiration, and remains imperceptible as long as the thorax is kept in the position of inspiration; in the carotid and femoral the wave becomes much smaller, the heart sounds continue uniformly. The individual in question enjoys very good health and is very well nourished. In his childhood he had pleurisy upon the left side. I may also mention that in a case of large effusion into the left pleura, observed at von Ziemssen's clinic also for some time, while the exudation filled the cavity entirely, and caused considerable displacements, the radial pulse disappeared almost entirely during inspiration. In all tliese cases the phenomenon of the pulsus inspiratione intermittens must be connected with a factor due to the alteration of the thorax during inspiration. I cannot assent to the idea expressed by Baeumler. He believes that the pressure which is rendered positive by the exudation within the thorax hinders the aspiration of blood during the act of expiration to such an extent that when the systole of the PNEUMOPERICARDIUM. 657 left ventricle occurs simultaneously with the act of inspiration, there is but a small amount of blood to be expelled. This condition cannot cause the paradoxical pulse, because the latter beats regularly during prolonged expiration, and always stops regularly during a pause in the position of inspiration, even if the pause is kept up as long as possible. In my opinion the inspiratory displacement of the thorax may produce, under different conditions, mechanical obstructions which result in the expulsion of a less amount of blood ; these may occur in the aorta, perhaps also in the subclavian, or at the origin of the vessels, and then the heart sounds are unchanged; or they may be in the heart itself, and then we find at the same time a diminution of its action. The production is favored by a weak, degenerated heart. Besides these mechanical hindrances in the circulatory system, caused by the act of inspiration, the phenomenon of the pulsus inspiratione intermit- tens may also be produced by obstruction to the entrance of air into the lungs, for the inspiratory augmentation of the negative pressure (suction) within the thorax opposes the supply of a proper amount to the aortic system (see Baeumler, 1. a). In this case there is an exaggeration of a normal relation, for even under normal con- ditions the sphygmograph shows that the negative pressure within the thorax during inspiration can cause a slight diminution of the wave, as Riegel and Sommerbrodt have shown.1 Pneumopericardium. Voigtel, Hanab. der path. Anat. 2 Bd. Halle. 1804:.—Bricheleau, Obs. d'hydropneu- mopericarde. Arch. gen. de Med. Tom. IV. 1844. p. 334.— Horst, Hufeland's Journ. Jan. 1844.—IF. Stokes, Dis. of the heart and the aorta. Dublin. 1854. p. 21.— Chambers, Lond. Journ. July, 1852.—Feine, Diss, pericardii laesi cas. rar. sist. conatum cum simil. etc. Lips. 1854.—Sorauer, De Hydropneumopericardio diss. Berol. 1858. — 0. Wyss, De fistula pericard. comment. Vratisl. 1866.— Demarquay, Essai de Pneumatologie medicale. Paris. 1866. p. 363.—Tiltel, Fall von Pneumopericardium. Deutsch. klinik 37. 1860.—J. Beckers, De Pneumo- pericard. Diss. Greifswald. 1860.—Bodenheimer, Ein Fall von Pyopneumoperi- card aus der klinik des Prof. Dr. Munk in Bern. Berl. klin. Wochenschr. 1865. 35.—Morel-Lavallee, Rupt. du pericarde; bruit de roue hydraulique, bruit de moulin. Gaz. Med. de Paris. 1864. No. 46.—C. Eisenlohr, Ein Fall von Pyo- pneumoperic. Berl. klin. Wochenschr: No. 40. 1873.—Saexinger, Pneumoperi- card. bedingt durch Perforation eines runden Majengeschw. Prag. med. Woch- enschr. 1865. —Fetzer, Ein Fall von Pneumopericard. Wurtemb. Medic. Corresp.- Bl. 1874. No. 40. See also handbooks and textbooks on diseases of the heart. The presence of air in the pericardial sac is an exceedingly 1 Berl. klin Wochenschr. 1876. No. 26. S. 369; and Ein neuer Sphygmogr. Bresl. 1876. VOL. VI.—42 658 BAUER.—DISEASES OF THE PERICARDIUM. rare occurrence. The older physicians considered pneumoperi- cardium, except the cases due to a traumatism, as an idiopathic affection, or they explained the accumulation of gas by the supposition of spontaneous decomposition of a pericardial effu- sion. The possibility that pneumopericardium could arise by the development of gas in a decomposing ichorous exudation was maintained by the most trustworthy observers—Laennec, Skoda, Stokes, Rokitansky, Traube and others. Duchek and Fried- reich also defended the opinion that most cases of pneumoperi- cardium were due to the development of gas in ichorous exuda- tions, and in the two cases recorded and observed by them, no other cause could be found, although the search was thorough. To express a doubt of the demonstrative value of such consci- entious observations, in which another explanation scarcely seems allowable, is always somewhat questionable. But, not- withstanding its improbability, in the face of the results of the anatomical investigation, the possibility must be borne in mind that there was a connection through which the air entered from outside—from the pleural cavities into the pericardium. The reasons why such observations, apparently so convincing, must be doubted, are of course mainly theoretical, but they are substantial enough to make the production of pneumopericar- dium by the development of gas in a decomposing exudation appear extremely improbable. The analysis of the gas collected in the pericardium, in those cases in which the anatomical examination makes it seem probable that it has been developed there, will determine whether this view is correct or not. Huefner has recently examined gas taken from a pyaemic abscess in the thorax, with the following result: Carbonic acid gas and sulphuretted'hydrogen........... 1.05 per cent. Oxygen............................................ 14.50 " Nitrogen........................................... 84.45 " This result agrees with the values found by Dressier in his analyses of gases of the same kind taken from an encapsulated peritoneal exudation, an ovarian cyst, and a cyst of the thyroid gland, to this extent that the quantity of the indifferent nitrogen was almost the same. Dressier found more carbonic acid gas and less oxygen in the gases he examined. PNEUMOPERICARDIUM. 659 nuefner concludes from these results, in opposition to the opinion held by- Dressier, that the presence of gas was due to the entrance of atmospheric air with subsequent oxidation. Future examination of the gas will determine whether its presence in a serous cavity can result from the decomposition of an exudation or not. In cases in which the symptoms of a pneumopericardium appear during life, and which end in recovery, it is not justifia- ble to suppose there has been a development of gas in an exuda- tion, difficult as any other explanation may be. The cases of purely spontaneous development of gas without the presence of a decomposing exudation must be considered as mistakes. Perforation of the pericardium occurs by suppurative de- struction from within outwards, when there is a purulent exuda- tion within the pericardium, and from without inwards likewise by advancing ulceration and destruction, also by neoplasms extending from the mediastinum, from the oesophagus, or, after destruction of the diaphragm, from the abdominal viscera to the pericardium, and finally by aneurisms. If the opening estab- lishes communication between the pericardial sac and a cavity containing air, or if it opens externally, air can enter into the pericardium. The entrance of air may be aided by positive pressure, such as is exerted upon it in the stomach, the lungs, or the pleural cavity when pneumothorax is present; it is also helped by the elastic traction of the lungs upon the pericardium, and the diminution of the heart during the systole. In Chambers', Becker's, and Tuetel's cases ulcerative perforation took place from the oesophagus; McDowel saw a case of perforation from a cavity, Eisenlohr one from a pyopneumothorax, and Saexinger one from a gastric ulcer into the pericar- dium. In a case given by Graves an abscess of the liver communicated at the same time with the stomach and pericardial sac. The pericardial sac can also be opened by injuries of all kinds, so that air can penetrate into it. According to von Bamberger's testimony the entrance of air does not necessarily take place in every case of penetrating wound of the peri- cardium. Feine and Bodenheimer have recorded cases due to penetrating wounds. Thompson and Walshe saw pneumopericardium follow opening of the pericardial sac from the oesophagus by a knife that had been swallowed; Morel-Lavallee saw 660 BAUER.—DISEASES OF THE PERICARDIUM. it caused by penetration of a fractured rib into the lung and pericardium. Morel- Lavallee and Steiger saw air enter the pericardial sac after contusions and crushing. The relations are, without exception, such that inflamma- tion of the pericardium is set up at the same time. The character of the exudation for apparent reasons is purulent, hsemorrhagic, or ichorous (pyopneumopericardium). The peri- cardium may be more or less distended and stretched by the accumulated gas, and consequently the air escapes with a hiss- ing sound when the sac is opened. The gas, as a result of its specific gravity, always occupies the upper portion. Retraction of the lungs and depression of the diaphragm occur to an extent corresponding to the distention of the pericardium. In rare cases pneumatosis of the pericardium occurs as a cadaveric incident, in which case the serous membrane presents a parch- ment-like dryness, the result of evaporation (Foerster). The subjective symptoms in pneumopericarditis are not char- acteristic ; on the other hand, the objective signs are so prom- inent and striking that they can hardly be misinterpreted. The patients complain usually of severe dyspnoea; cyanosis also is present; and if the condition, as is often the case, coin- cides with severe symptoms of collapse, the skin is pale with a bluish tint. The pulse is small, also irregular; delirium and fainting fits occur; sometimes the patients complain of nothing, and are only very weak and indifferent. Usually also there is sleeplessness, caused partly perhaps by the loudness of the heart murmurs. High fever or chills are sometimes observed, which, however, like the profuse sweats, diarrhoea, etc., must be attributed to the original lesion and not directly to the pneumo- pericarditis. Dysphagia was observed by Eisenlohr. The chest-wall may be noticeably prominent in the region of the heart when it is soft and the pericardium is greatly distended by air. The apex-beat varies, it may be weakened or absent; sometimes pulsation can be felt in several intercostal spaces. The crackling of air bubbles, synchronous with the movements of the heart, can be perceived by the hand laid upon the breast. In Graves's case a loud metallic ring was heard with each beat of the heart. The faintness of the apex-beat disappears as soon as the patient sits up and bends forward. PNEUMOPERICARDIUM. 661 The signs obtained by percussion are very characteristic. The note over more or less of the region of the heart is purely tympanitic with metallic resonance, the height of which cor- responds to the smallness of the cavity containing air. Gerhardt noticed in one case that when rapid and continuous percussion was made at one point the metallic resonance became higher and lower, following the rhythm of the heart, as the result of the changes in the shape of the body of air contained in the peri- cardium. According to Feme's observation the note in the region of the heart became duller with each systole, because during it the heart is situated further forward and downward against the thorax and presses back the air, and during the diastole the note again became clearer. The cracked-pot sound has been repeatedly noticed; whether this can occur in a closed pericardium without an open communication, as is claimed, appears doubtful. The air in the pericardial sac is always found in the highest portion, the heart and the exudations tha't may be present always sink downwards. When the patient is seated, therefore, the clear tympanitic note is limited below by a non-resonant one, and the limits change suddenly and remarkably with change of the patient's position. In the horizontal position upon the back the portion of the pericardium containing air must be spread to the greatest extent against the anterior wall of the chest, and this extent grows constantly less as the patient rises and bends forward. In the same way the contents of the pericardium arrange themselves according to weight in the different lateral positions of the patient. It is not certainly known, but it is to be expected a priori, that a succussion sound can be obtained by shaking the patient, as in hydro-pneumothorax. The signs of pneumopericarditis obtained by auscultation are very surprising and peculiar, for they are remarkable for their intensity as well as their character. As a rule several different sounds can be heard, and indeed they are usually so loud l that 1 I have heard very loud endocardial murmurs (naturally without metallic reso- nance) by chance within a short time in three cases of aortic insufficiency, and they were diastolic. These murmurs could be heard at a distance of ten steps from the bed. 662 BAUER.—DISEASES OF THE PERICARDIUM. they can be perceived not only by the patient, but also by those standing at some distance ; thus in Stokes's case the sleep of the patient himself and of his wife was disturbed by the murmur. The heart sounds are unusually loud and accompanied by a clear metallic ring like a chime (Friedreich). It is of course said that in many cases the heart sounds cannot be heard, but this can only be the case when other sounds conceal them. In most cases a large amount of liquid exudation is present at the same time in the pericardial sac, and this is moved about by the heart in the space containing air, and is agitated and mixed with it. In this way there are produced loud sounds accompanied by a metallic ring, splashing and spluttering, gurgling and rattling, and consequently known as water-wheel sounds (bruit de roue hydraulique, bruit de moulin). In the case observed by Oppolzer in Pitha's clinic the sound was not unlike that produced by shaking shot in a shot-pouch. Drop- ping is heard as in pneumothorax. If pericardial friction is present it is also accompanied by metallic resonance. As compared with these symptoms, those of pericarditis, which are present at the same time, retire to the background. If there is a large purulent effusion it naturally helps materially to greatly oppose the circulation and respiration, and to make the prognosis exceedingly unfavorable. The collection of air itself in the pericardium can of course exert an influence by its great tension upon the filling of the ventricle during the diastole and also upon the retraction and compression of the lungs. What makes the progress and termination of the affection especially unfavorable is of course in most cases the original pro- cess which in itself often gives a purulent, ichorous character to the consecutive pericarditis. We can form no opinion as to the nature of those cases which have terminated favorably;—of four- teen cases collected by Friedreich ten ended fatally. Hitherto these have been usually explained as due to the development of gas in the exudation ; but one would suppose that a decom- posing exudation in the pericardium would certainly prove fatal. In the cases that recovered it must certainly have been atmos- pheric air which penetrated in some unknown way into the peri- PNEUMOPERICARDIUM. 663 cardium and was there reabsorbed, as we know can be done in the course of a few days. The prognosis of pneumopericarditis is consequently unfavor- able ; those cases must be considered certain to end fatally in which the original process produces dangerous complications. Most favorable in any case are those due to mechanical trau- matisms. The diagnosis of pneumopericarditis seems as a rule to offer no great difficulties. It may be confounded with a greatly dis- tended stomach, which may produce metallic sounds in the region of the heart, but which usually are independent of its movements. In many cases of this kind, however, the action of the heart produces, by a sort of internal percussion of the stom- ach, systolic metallic sounds and even rales of metallic timbre (Gerhardt). The distention of the stomach, which can be easily recognized, the normal area of dulness, the apex-beat at the nor- mal spot, or a little to the outside of it, make it easy to avoid a mistake. Metallic sounds dependent upon the movements of the heart can also be heard in cavities near the apex of the heart. It is not difficult to discriminate them : the heart occu- pies its normal position, rales are also produced in the cavity by respiration, and by opening and shutting the mouth the hight of the percussion note is changed (Gerhardt). Encapsulated pneu- mothorax near the heart is most likely to present symptoms similar to those of pneumopericarditis. Still in such cases the precordial dulness can usually be made out, even if displaced ; and on auscultation, besides the metallic ring of the heart sounds, the resonant phenomena which accompany the respira- tory sounds can especially be made out. The treatment must be directed to the original lesion and the consecutive pericarditis. As for the latter, the principles already laid down hold good; oppose the adynamic symptoms by strengthening and stimulating measures, regulate the action of the heart by digitalis in small doses, place ice bags over the heart. Narcotics must be used to control the pain, restlessness, and sleeplessness as well as the dyspnoea. As soon as the distention of the pericardium becomes very 664 BAUER.—DISEASES OF THE PERICARDIUM. great, the question must be considered whether it is not proper to remove as much as possible of the air from the pericardium by puncture with a fine trocar. The procedure may be considered as free from danger ; the precaution must only be taken to intro- duce the trocar while the patient lies upon his back. If the escaping gas shows by its odor—like sulphuretted hydrogen—that processes of decomposition are going on in the pericardium, or if it is accompanied by decomposing liquid, then the performance of a radical operation and the washing out of the pericardial sac with a disinfecting liquid is decidedly indicated. But this should be determined upon only in case the fundamental lesion offers some chance for the preservation of life. Hydropericardium. Schellhammer, Diss, de aqua pericardii. 1694.—Fr. Hoffmann and Graetz, Diss, de hydrope pericardio rariss. Hal. 1697. v. Opp. Suppl. II. 2.—Merker, Diss, de hydrocardia. Ultraj. 1711.—Landvoigt, Diss, de hydr. pericard. diag. Hal. 1798.—Heinecke, Diss, de hydr. pericard. Erf. 1709.—Modes, Essai sur l'hy- drod. du pericarde. Paris. 1808.—Schuh, Oesterr. med. Jahrb. Bd. XXIV. Schmidt's Jahrb. XXXII. S. 196. —Skoda, Oesterr. m6d. Jahrb. 1841.— Philipps' Jahresb. 1841. S. 39.— Waschsmuth, Virch. Arch. Bd. VII. 330. Virchow, Ges. Abhandl. S. 108. u. Spec. Path. Bd. I. S. 205. See also the various manuals and text-books. In the pathology of former times dropsy of the pericardium played an important part, since not only was no distinction made between inflammatory effusions and serous transudations, but the affection was also said to occur as a metastasis in a great variety of acute and chronic affections, and to be the cause of their unfavorable result. In recent pathology pericardial dropsy occupies a different position, but in many places at least the old view is still the popular one, and the symptom is still regarded as an unmistakable harbinger of death. By hydrops pericardii (pericardial dropsy, hydro-pericar- dium, hydrocardium), we are to understand an accumulation of serous fluid in the pericardium occurring independently of in- flammation. Tliese terms, however, in view of the fact that a HYDROPERICARDIUM. 665 certain amount of fluid is met with in most autopsies, are appli- cable only to those cases in which the dropsical accumulation is excessive. The hypothesis has been frequently advanced that a certain amount of liquor pericardii is present even during life, for the purpose of filling the vacuum and facilitating the move- ments of the heart. I cannot agree with this view ; on the con- trary, it seems to me that even the normal liquor pericardii is to be regarded as a transudation, which has escaped during the agony, or after death, from the vessels and from the heart itself, particularly from the frequently tensely distended right ventri- cle. This transudation continues for a time immediately after death, so that more fluid is found in the pericardial sac when the autopsy is made at a late period than when it is made early. The quantity of fluid depends, moreover, upon the duration of the agony, and upon the final cause of death, being increased in those affections which are accompanied by great congestion of the coronary veins, as for instance emphysema, distortion of the thorax, phthisis, death from suffocation, valvular diseases, etc. Fluid is not found in the pericardium at every autopsy, but it occurs in most cases to the amount of from half an ounce to an ounce. Under favorable circumstances, as much as three ounces and upwards may be present without being necessarily regarded as anything more than a result of the agony and post-mortem changes. Such cases have no pathological significance unless it can be shown that the fluid was present during life (v. Bamber- ger). The transudations which take place during life are sometimes very copious, amounting to a pint and a half or more, and Corvisart reports the scarcely credible quantity of eight pounds. The transudation is composed, as a rule, of a clear yellowish or greenish serum ; occasionally, however, it is somewhat turbid from the presence of desquamated epithelium, which has under- gone fatty degeneration. Some of the coloring matter of the blood may also be mixed with it, giving it a reddish or brownish tinge, and this escape of heematin may take place after, as well as before, death. The reaction of the fluid is alkaline. The solid ingredients of the effusion are the same as those of 666 BAUER.—DISEASES OF THE PERICARDIUM. the blood-serum, but in different relative proportions. The percentage of solids also varies considerably in different cases. The fluid which is effused into the pericardial cavity after death must always be regarded as the product of a filtration, under increased pressure, from the blood-vessels and cavities of the heart; while the fluid contains less albumen than the blood- serum on account of the difficulty with which albumen passes through membranes. The percentage of albumen will depend in these cases upon the force of the pressure, the duration of the process, and the composition of the blood. When the effusion takes place during life, its composition is the result of a number of complex processes (see E. Wagner's Manual of General Pa- thology).1 The fluid probably always contains fibrogenous matter, and therefore the occurrence of spontaneous coagulation in the serous fluid does not warrant the separate classification of a lymphatic or fibrinous dropsy. Urea is also present in the serous fluid, especially in renal diseases, together with other products of decomposition. In general icterus the coloring matter and acids of the bile are also found. The upper surface of the pericardium presents more of the characters of inflammation, and has an opaque, pale, dull- white appearance. Formerly there was recognized also an inflammatory dropsy of the pericardium, which included those cases of pericarditis where the effusion was chiefly of a serous character—and partially organized products of inflammation were found upon the serous surfaces (chronic pericarditis), or, perhaps, only trifling changes of an inflammatory character are 1 Composition of the pericardial effusion : Wachsmuth. Wagner. Gobup-Besanez. Water.......95.37-97.34 Solids.......'2.66- 4.63 Albumen.. 1.43- 3.01 Other ingre-dients... 1.23- 1.64 Water............96.51 Solids............. 3.49 Albumen.......2.915 Water.............95.51 Solids............. 4.487 Fibrin..........0.081 Albumen........ 2.468 Extractives......1.269 Inorganic Salts.. 0.948 HYDROPERICARDIUM. 667 noticed. In cases of the latter kind the original affection may have been a simple effusion, in the course of which inflammation has supervened ; but in all such instances, where inflammatory changes are noticed, the inflammation rather than the dropsy is the object of chief concern. At the same time it maybe diffi- cult in individual cases to decide which is the more important element. The cavity of the pericardium is dilated in proportion to the amount of fluid, and its fibrous layer is thinned, or occasionally, when the dropsy has continued for a long time, thickened. In chronic cases, the subserous fat about the heart disappears, the subserous cellular tissue appears oedematous, and the endothelia are relaxed, swollen, and of a granular opacity. The muscular substance of the heart is pale and flabby. In the more copious effusions the lungs are found compressed, and the diaphragm forced downwards. The causes of pericardial dropsy are very numerous, but the affection is always secondary and never primary and idio- pathic.1 When it makes its appearance during life, and before the occurrence of the agony, it is either due to a stasis in the veins and lymphatics of the heart and pericardium, or it is merely one of the symptoms of a general dropsy. When the reflux of the blood from the veins of the heart and pericardium is impeded by stases in the lungs, or in the heart itself, the passive congestion thus induced may give rise to a dropsy of the pericardium ; the same result may be produced by atheromatous disease of the coronary arteries. In rare cases also, the contractions of bands of connective tissue in the thorax, or neoplasms in the mediastinum or in the heart, may derange the circulation in such a way as to induce a serous effusion into the pericardium. The hypothesis has also been advanced that fluid may be effused into the peri- cardial cavity to fill the vacuum produced in the chest in cases of shrinking of the lungs, atrophy of the heart, and particularly where traction results from the adhe- 1 Duchek found dropsical effusions in the pericardium in 13 per cent, of his autop- sies, Giinsburg in only 7.4 per cent., and, in fact, most frequently in pulmonary tuber- culosis. 668 BAUER.—DISEASES OF THE PERICARDIUM. sion of the pericardium to the lungs. The occurrence of such a hydrops ex vacuo is especially insisted upon by v. Bamberger, who advocates this view, as a result of atrophy of the heart arising from acute dyscrasic processes, such as cancer, tuber- culosis, etc. Giinsburg, and afterwards Friedreich and others, have shown, how- ever, that such a genesis of pericardial dropsy is impossible, because the dilatation of the lungs, the retraction of the thorax, and the ascent of the diaphragm would naturally prevent the occurrence of a vacuum. In the cases mentioned hitherto, the hydrops pericardii is dependent upon local conditions. It may occur, moreover, as one of the symptoms of a universal dropsy, or as the result of a watery condition of the blood, particularly in parenchymatous nephritis, also in tuberculosis, cancer, and other cachectic condi- tions. But, at the same time, it should be remarked that drop- sical effusions do not occur so frequently in the pericardium as in other serous cavities, probably on account of the influence of the incessant muscular contractions of the heart in promoting the circulation of the blood and lymph. The smaller quantities of serous effusion present during life no symptoms of any kind, and remain undetected until the fluid has accumulated in greater amount. The physical evidence consists chiefly of the results of percussion, and, as regards the quantity of the fluid necessary for recognition, the same rule applies as in the case of pericardial exudations. In the latter, however, the results of percussion are substantially confirmed and their significance certified by the presence of friction mur- murs and subjective symptoms; whereas, in pericardial effu- sions friction can never occur. When the amount of effusion is small, therefore, there is greater danger of drawing erroneous conclusions from the percussion signs than is the case in ex- udations. Percussion shows an increase of the cardiac dulness corre- sponding to the distention of the pericardium, the conformation of the distended sac being the same as in pericardial exudations, viz., that of a triangle with its base directed downwards. Here also we have an enlargement of the cardiac triangle and an in- crease of dulness on the patient's changing from a recumbent to an upright position, or on bending forwards ; and this sign is particularly valuable in cases where, in consequence of a coex- IIYDROPERICARDIUM. 669 isting pleuritic effusion, the broadening of the triangle can be detected only at the apex, which is pushed considerably upwards in the upright posture. In serous pericardial effusions there is of course an absence of inflammatory changes upon the external surface of the pericardium, and therefore, although the borders of the lungs are forced backwards by the distended pericardium, adhesions do not occur. The respiratory mobility resulting from this fact is, however, of no importance as a means of distinguishing this condition from pericardial exudation. The character of the apex-beat in hydropericardium is also the same as in pericardial exudations, the beat becoming more feeble, or disappearing altogether when the accumulation of fluid is large. The sounds of the heart grow duller, and in very rare cases become entirely inaudible. Certain symptoms, such as a visible undulatory movement, fluctuation on pal- pation in the cardiac region, etc., have been described by some writers, particularly the older ones, as occasioned by the presence of fluid in the pericardium ; but these signs are just as uncommon in effusions as in exudations. According to Hope, the apex-beat, when it can be detected in spite of a large accumulation of fluid, does not coincide with the systolic sound of the heart, on account of the resistance which the fluid opposes to the cardiac movements. The influence of the pericardial dropsy upon the cardiac movements, the circulation and the respiration, can be estimated only in those cases in which these functions are not seriously impaired by the coexistence of a general dropsy or by the funda- mental disease. In such cases the mechanical influence of the fluid accumulation must manifest itself in the same way as in the case of an exudation. On the other hand, there is an absence of all the symptoms which are produced by inflammation of the serosa, among the most important of which are the acute de- rangements of nutrition on the part of the cardiac muscle. Where the dropsy continues for a long time it is possible that the pressure of the fluid may impair the nutrition of the cardiac muscle, and thus gradually induce atrophy and degeneration. The mechanical effects of large pericardial effusions are mainly these : a lowered pulse-wave, a diminished filling of the arteries, a lessened secretion of urine, venous congestion, cyano- sis, compression of the lungs, and depression of the diaphragm. As a result of these conditions, difficulty in breathing ensues, 670 BAUER.—DISEASES OF THE PERICARDIUM. which may increase to a continuous orthopnoea, with extreme dyspnoea in the horizontal position. The patient experiences a sensation, not only of anxiety and difficulty in breathing, but also of oppression and weight in the chest. When the fundamental disease is of such a character as to itself induce symptoms of this kind, it is impossible to deter- mine what share in their production is taken by the pericardial dropsy. On the other hand, the fundamental disease, by occa- sioning a high degree of anaemia, may even assist in moderating the intensity of the dyspnoea, etc. Moreover, the rapidity with which the effusion takes place will modify in an important de- gree the severity of the subjective symptoms. As regards the diagnosis of hydropericardium, the first object is to ascertain whether the existing physical changes are in fact occasioned by a distended pericardium; and here we are to be guided by the same rules as in inflammatory pericardial effusions. In the differential diagnosis from a pericarditis exsudativa we must inquire whether any local or general conditions can be found which might give rise to a dropsical effusion, and especially whether dropsy exists in any other part of the body. When such a condition is present, the absence of friction sounds, of fever, and of all inflammatory symptoms, is a very important indication. The prognosis is very unfavorable, because the conditions which produce the dropsical effusion are almost invariably of a permanent character ; in fact, we generally have to deal with an incurable fundamental disease, of which the hydropericardium is merely a comparatively unimportant consecutive symptom. In- asmuch, however, as it is not at all uncommon for the general dropsy of kidney and heart diseases, etc., to disappear tem- porarily, it is reasonable to suppose that when such a happy result occurs the pericardial dropsy may also be absorbed. Such an occurrence, however, will be rarely observed, because the effusion does not usually take place until a disappearance of the general dropsy is entirely out of the question. A permanent cure may be anticipated if the dropsy be dependent upon a transitory hyperaemia. H^EMOPERICARDIUM. 671 In general dropsy a large pericardial effusion will unquestion- ably contribute largely to the fatal result, and may even induce it directly by impeding the cardiac and respiratory movements. The treatment must be directed to the fundamental disease. In many cases, therefore, the same remedies are to be used as in general dropsy, and wmere the latter declines under the use of diaphoretics and diuretics, the same beneficial effect will extend to the pericardial effusion. Cardiac tonics are also indicated. In copious effusions, which involve a direct danger to life, puncture of the pericardium is entirely justifiable, and is unat- tended with much risk, if care be taken to exclude air. Hemorrhage into the Pericardial Cavity. Hsemopericardium. This condition occurs, independently of wounds, in rupture of the heart. The quantity of blood poured out into the pericardial cavity will vary considerably, according to the manner in which the rupture takes place. In large lacerations the extravasation is not so copious as one would expect (perhaps a pint), partly because death ensues rapidly from acute anaemia of the brain or from a momentary arrest of the heart's action, and partly be- cause the pericardium opposes more resistance to a sudden than to a gradual distention. Where the laceration is small the effu- sion of blood takes place more gradually, its quantity is much more considerable, and death results more tardily. Pericardial hemorrhage may also be produced by rupture of the coronary vessels, where these have been previously diseased, and particularly where aneurisms have formed upon them. Aneurisms of the aorta may likewise burst into the pericardial sac. The physical signs of pericardial hemorrhage consist of dis- tention of the pericardium, together with the symptoms of acute anaemia and paralysis of the heart. Inflammation of the serosa will ensue as a complication only where the case does not ter- minate in sudden death, 672 BAUER.—DISEASES OF THE PERICARDIUM. A certain amount of extravasated blood is frequently found in exudative pericarditis ; and in some inflammations, especialty the scorbutic forms, the fluid contents of the pericardium may present the appearances of pure blood. Free Bodies in the Pericardium. Lanzoni, Miscell. Natur. Curios. Dec. 111. Ann. VII. et VIII. Obs. 75. p. 119.— Kussmaul, Wiirzb. med. Zeitschr. V. Bd. 1864, and Steinlein, Ein Dorn im Herzfleisch und ein freier Korper im Herzbeutel. Diss. Erlangen. 1868.—Hyrtl, Ein freier Korper im Herzbeutel. Sitzungsbericht der K. K. Akad. der Wis- sensch. 51. Bd. 23. Marz. 1865.—Klob, Freier Korper im Pericard. Zeitschr. der K. K. Gesellschaft der Aertzte zu Wien. N. 49. 1860.—Rokitansky, 1. c. Free bodies within the pericardium have been met with on only a few occasions. Some of them were soft and smooth sub- stances, as large as a pea or bean, while others were of a firm, fibroid consistence, sometimes stratified, and even calcified, either at the centre or in toto—cardiac calculi. They probably originate in the formation of precipitates or fibrinous coagula- tions around a foreign body, or in the formation of polypoid growths, which ultimately become detached. No characteristic symptoms have been observed during life. Pericardial hydatids are of very rare occurrence. A case of this kind has been described by Barlow.' 1 Pathological Transactions, 1855. WHOOPING-COUGH. (TUSSIS CONVULSIVA.) STEFFEN. VOL. VI—43 WHOOPING-COUGH. BIBLIOGRAPHY. Adams, Lancet, Feb. 5, 1870.—Ballantyne, Lancet, June 25, 1870.—Bisset, Medical Essays and Observat., 1776, p. 174.— Todd, Med. Times and Gazette, Mar. 4, 1854.— William Butter, A Treatise on the Kink-cough. London, 1773.—L. Chalmers, An Account of the Weather and Diseases of South Carolina. Lond., 1776.—i'V. 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Journ., Aug., 1872.—J. S. Hough, How to Prevent Paroxysmal Coughs, Amer. Journ. Med. Sci., April, 1873.— B. F. Dawson, Quinine in Whooping-cough, Amer. Journ. of Obstet., Feb., 1873.—Meigs and Pepper, A Practical Treatise on the Diseases of Children, 5th ed. Phila., 1874.—J. Bordley, Hydrate of Chloral in the Treatment of Pertussis, Amer. Journ. Med. Sci., April, 1874.—A. Flint, A Treatise on the Principles and Practice of Medicine. Phila., 1857.—D. Maclean, On the Open- Air Treatment of Whooping-Cough, Glasgow Med. Jour., Nov., 1872.—D. Carlos, Treatment of Whooping-Cough by Carbolic Acid, Lond. Med. Record, Nov. 15, 1875.—R. Harrison, Treatment of Whooping-Cough with Carbolic- Acid Inhalations, Brit. Med. Jour., 1875, II., p. 489.—R. Bell, Treatment of Whooping-Cough by Iodide of Silver, Obstet. Journ. of Gt. Brit, and Ire., III., p. 589.—R. J. Lee, Treatment of Whooping-Cough with Carbolic-Acid Vapor, with Description of a Steam Draft Inhaler, Brit. Med. Journ., 1875, H., p. 425. Ballonius, Epidem. lib. Const, sestio, 1578. Genev., 1724, I.—Billard, Traite" des maladies des enfans, etc., 1828, p. 535.—Blaud, Revue med., 1831, T. I., p. 233.—Beau, Gaz. des hopit., 1861, No. 48, und Archiv. gen6r., Sept., 1856.-— Blache, Diction, de medec, en 30 vol., T. IX., p. 24, und Archiv. gengr., 1833, Oct. et Nov.—Blache et Guersent, Union med., 1853, p. 196.—Bell, Diction- BIBLIOGRAPHY. 677 naire des etudes medicales, T. XIV., p. 226.— Barrier, Maladies de l'enfance, T. I., p. 135.—Bouchut, Traite des malad. des nouveau-nes, etc., 1862.—De la Berge et Monneret, Compendium de medec pratique, T. II., p. 526, 1837.— Barthez et Rilliet, Maladies des enfants, 1843, II., p. 207.—J. Capuron, Abhand- lungen iiber die Krankheiten der Kinder. Uebersetzt von B. Puchelt, 1821, S. 339.—A. Clermont, Employment of the Arseniate of Iron, L'Union, 15, 1875. — Constant, Gaz. med. de Paris, 1836, p. 532, und Bulletin therapeutique, VI., p. 229.—A. Duges, Dictionn. de medec et de chirurg. pratiq., T. V., p. 487.—Desruelles, Traite de la coqueluche, 1827.—Finaz, Revue medic, T. II.— Uuersent, Dictionn. de mSdec, en 21 vols., T. VI., 1823.—Nat. Guillot, Union medic, 1853, p. 184.—Guibert, Recherches nouv. sur le croup et la coqueluche, 1824.—Gendrin, Gaz. me*dic de Paris, 1850, 7. Dec.—Gallerand, Diss, sur la toux convuls. des enfants, 1812.—Hervieu.v, Journal fiir Kinderkrankheiten, 1862, S. 114.— Jacqnart, Gaz. med. de Paris, Mars, 1862, No. 13.—Laborde, Gaz. des hopit., 1865, No. 38.—Luroth, De la coqueluche et de son traitement, 1849.—Laennec, Traite de l'auscultation, 2. edit., T. I., p. 216.—J". Lieutaud, Synops. univers. prax. med., 1765, T. I., p. 493.—Mignot, Union med., 3. Juillet, 1862.—Montan, Sedillot journ. de mgd., 1812, p. 384.—Ozanam, Archiv. genSr., 1854, T. I.—J. A. P. Ozanam, Histoire m6d. general et particul. des malad. epid., 1818, T. II, p. 140.—Roger, De l'emphyseme generalise" pul- monale, mediastin. et sous-coutane, Arch. ggn. de med. Aout, Sept., Oct., 1862; Bulletin de I'acad., Dec, 1852; Gaz. des hopit, 1863, No. 3.~Rostan, Cours de med. clinique, T. II., 1830—Trousseau, Memoire sur la coqueluche, Journ. de med., Janvier, 1843; Clinique medic de l'hotel Dieu de Paris, T. I., 1861, p. 495.—Triquet, Gaz. des hopit., 1863, No. 9.—Fallami, Gazz. med. ital. Venet., 1866, 5 Magg.—Aless. Gambarini, Schmidt's Jahrb., Bd. 83, S. 326.— darelli, Gaz. med. Stat. Sard., 1851, No. 7.—Zaniboni, Gazz. medic Lomb., 1864, No. 43.—Brunniche, Bibliothek for Laeger, Jan., 1867.—Nic. Rosen von Rosenstein, The Diseases of Children and their Remedies. Translated from the Swedish into English by Sparrman. London, 1776. JJ. A. Aaskow, Sammlung auserlesener Abhandlungen, Bd. IV., S. 512.—ATberti, Diss, de tussi infant, epid. Halle, 1728.—Aberle, Tuss. convuls., etc., 1843.— Archner, Froriep's Notizen, Bd. II., S. 272, Bd. III., S. 336.— Atenstadt, Medic. Centralzeitung, 1856, No. 50.—J. H. F. Autenrieth, Versuch fiir die praktische Heilkunde, 1807, Bd. I., Heft 1-2.—J. H F. Autenrieth und J. G. F. v. Bohnenberger, Tubingen, Blatter fiir die Naturwissenschaften und Arzneikunde, 1813, B. I., S. 23.—Bednar, Krankheiten der Neugebornen und Siiuglinge, Bd. III., S. 48.—Biermer, Handbuch der spec. Pathol, und Therap. von Virchow, Bd. V., Abth. I., S. 531, with numerous references to the literature of the subject.—Breidenbach, Centralblatt fiir die medic. Wissensch., 1869, No. 34.— Binz, Jahrb. f. Kinderheilk., N. F., Bd. I., S. 235, und Bd. IV., S. 103.—/. B. Burserius, The Institutions of the Practice of Medicine. Translated from the Latin into English by Wm. Cullen Brown, in 5 vols. Edinburgh, 1802.—Peter Camper, Sammlung auserlesener Abhandlungen, Bd. XYIH., S. 126.—Canstatt, 678 STEFFEN. —WHOOPING- COUGH Handbuch der med. Klinik, Bd. IL, Abth. 2, S. 677,1847.—F. G. Danz, Versuch einer allgemeinen Geschichte des Keuchhustens, 2. Auflage, 1802.—Ebeling, Dissertat. de tuss. convuls. Gottingen, 1768.—Ettmuller, De morbis infant, Opp. omn., P. II., p. 1, 1685.—Ferber, Jahrbuch fiir Kinderheilkunde, N. F. III., S. 229.— Faber, Wurtemb. Correspondenzblatt, 1834, Nos. 19-20. — C. B. Fleisch, Handbuch iiber die Krankheiten der Kinder, 1804, B. II., S. 399.— Flugel, Schmierkur gegen Keuchhusten, Blatter fiir Heilwissenschaft, 16, 1873. —Friedleben, Beitrage zur Lehre vom Keuchhusten der Kinder, Archiv fiir physiol. Heilkunde, Bd. XII., Heft 3^1, 1853.—J. Frank, Prax. med. univ. prase, P. IL, Vol. IL, Sect. 1, p. 825, 1823.—J". A. P. Gesner, Sammlungen und Beobachtungen aus der Arzneigelehrtheit, 1771, S. 199.—Chr. Girtanner, Abhandlung iiber die Krankheiten der Kinder, etc., 1794.—Gerhardt, Lehrbuch der Kinderkrankheiten, 1871, S. 378.—Gauster, Oesterr. Zeitschrift fiir prakt. Heilkunde, 1857, 30.—Gelmo, Jahrbuch fiir Kinderheilkunde, 1861, Heft 2.— Griva, Froriep's Notizen, B. XLIL, S. 48.—E. L. Heim, Vermischte med. Schriften, 1836, S. 213.— Hennig, Jahrbuch fiir Kinderheilkunde, HI., S. 49.— Hauke, Jahrbuch fur Kinderheilkunde, VI., S. 75.—Helmke, Jen. Zeitschrift, 1866, Bd. III.—Henke, Ueber mikroskopische Organismen in den Sputis keuch- hustenkranker Kinder und iiber die Wirkung der Chinin-Inhalationen bei dieser Krankheit, Deutsches Archiv fur klin. Medicin, 1874, XII., Heft 6.—Ad. Henke, Handbuch zur Erkentniss und Heilung der Kinderkrankheiten, 1818, Bd. II, S. 181.— Henoch, Beitrage zur Kinderheilkunde, 1861, S. 71, und N. F, 1868, S. 231.—Hinze, Hufeland's Journ. der prakt. Arzneik. und Wundarzneik., Bd. V., S. 906.— C. F. Holzhausen, Dissert, inaug. de tuss. convuls., 1815.—E. Horn, Archiv fiir medic. Erfahrungen, 1803 und 1805.—C. W. Huf eland, Bemerkungen iiber die natiirl. und geimpften Blattern zu Weimar im Jahre 1788, etc., 1793, und Journ. der prakt. Arzneik. und Wundarzneik., Bd. 4, 7, 9, 13, 15, und 20.—Fr. Hoffmann,. "Diss, de tussi convuls., 1732.—Fr. Jahn, Neues System der Kinderkrankheiten, etc., 1803.—D. F. Jahn, Klinik der chron. Krankheiten, 1821, Bd. IV., T. n., p. 375.— M. Jacobi, Horn's Archiv fiir medic. Erfahrungen, Bd. VI., S. 47.—J. H. W. Klinge, Etwas iiber den Keuchhusten, 1792.—J. G. Kbhler, De sede et natura tuss. convuls., 1818.— Krukenberg, Jahrb. der ambulat. Klinik in Halle, 1824, Bd. I., S. 288.— Kuttlinger, Bayerisch. arztl. Intellig.-Blatt, 1860, No. 2.—Keller, Jahrb. fiir Kinderheilk., VIII., S. 21.—Kbstlin, Archiv fiir wissenschaftliche Heilkunde, II., 4-5, S. 338, 1865.—J. F. B. Dentin, Beitrage zur ausiibenden Arzenei- wissenschaft, 1797, B. III., S. 25.—Lesser, Zur Behandlung des Keuchhustens, Allgem. med. Centralzeitung, 49, 1873.— W. Sachse, Das Wissenswiirdigste iiber die hautige Braune, 1810.—L. Letzerich, Virchow's Arch., Bd. XLLX., 1870, p. 530, and Bd. LX, 1874, p. 409.— Lebert, Handbuch der prakt. Medicin.—Lersch, Rhein. und Westphal. Corresp.-Blatt, 1844, No. 8.—Loben- stein-Lobel, Ueber Erkenntniss und Heilung der hautigen Braune, des Millar'- schen Asthma und des Keuchhusten, 1811, S. 143.—Lorey, Jahrb. fiir Kinder- heilk., N. F., Bd. V., S. 248.—D. C. J. Lorinser, Lehre von den Lungenkrank- HISTORY. 679 heiten, 1823, S. 429.—Lbschner, aus dem Franz-Josef-Kinderspital, II, 1868, S. 159.—A. Fr. Marcus, Der Keuchhusten, etc., 1816.—Matthaei, Horn's Archiv fiir med. Erfahrungen, Bd. III., S. 227.— Mellin, Beschreibung des Keuch- hustens zu Langensalza, 1770.—Mehlhose, Rust's Magazin, Bd. LI.—Fr. C. Meltzer, Abhandlung von dem Keuchhusten, 1790.—Memminger, Hufel. Journ., Bd. XIII, S. 189.—Monti, Jahrb. fiir Kinderheilkunde, N. F., Bd. VI, S. 103. — Oppolzer, Wien. med. Presse, Nos. 34-36.—L. Paldamus, Der Stickhusten, 1805.—J. Panzani, Beschreibung der Krankheiten, die in Istrien, 1786, ge- herrscht haben. Aus dem Italienischen von Fechner. 1801, S. 35.—Pohl, Progr. de analog, inter morbill. ettuss. convuls., 1789.—A. B. Polack, Diss, de tuss. convuls., 1829.—Rapmund, Das Chinin in der Kinderpraxis, etc., Deutsche Klinik, 7, 1874.—Rehn, Wiener med. Wochenschr., 1866, Nos. 52-53.—C. L. Reinhard, Spec. Nosolog. und Therap., 1834, B. I., S. 408.—.4. 67. Richter, Spec. Therap., 1821, Bd. VIII., S. 17.—Rosenthal, Die Athembewegungen und ihre Beziehungen zum N. vagus, 1862.—J. Schaffer, Hufel. Journ., Bd. VI., St. 2, and Ueber die gewohnlichen Kinderkrankheiten, 1803, S. 359.—Schenck, Observ. med. rar. nov., 1600, Lib. IL, p. 382.—M. Stoll, Ration, medendi, etc, P. IL, 1779.—67 Sprengel, Handbuch der Pathol., Bd. III., 1797, und Versuch einer pragmat. Geschichte der Arzneikunde, Bd. ni., 1794.—Steiner, Compend. der Kinderkrankheiten, 1873, S. 155, und Jahrb. fur Kinderheilk., N. F., Bd. V., S. 392.—Scoda, Allgem. Wiener med. Zeitg., 1860, No. l.—Stelzl, Oester- reich. Jahrb., 1844, August.—Schott, Wiirttemb. Correspondenz-Blatt, Bd. LX., No. 38.—Santlus, Joum. fiir Kinderk., XXIIL, 1854, Heft 4.—A. Steffen, iiber Inhalat. bei Tussis convuls., Journ. fiir Kinderkrankh., XLVII., S. 6, und Jahrb. f. Kinderheilk., N. F., Bd. IV., S. 227.—J". A. Unzer, Med. Handbuch, 1789, P. L, S. 228.—J. Wendt, Die Kinderkrankheiten systematisch dargestellt, 1822, S. 457.— Wilde, Zur Therap. des Keuchhustens, Deutsches Archiv fiir klinische Medicin, Bd. XIV., Heft 2.— Wintrich, Med. Neuigkeiten, 1858, S. 63, and 1861.— Zitterland, Rust's Magaz., Bd. XXH, p. 300. Finally, I cite the Handbook of Historico-Geographical Pathology, by Hirsch. In the second volume, 1862-64, p. 103, will be found the history of whooping- cough treated of in the greatest detail, with the very abundant literature which belongs to it. The literature of whooping-cough has already increased to such proportions, that in the foregoing list space could be found only for what was most important History. It cannot be determined with certainty when whooping-cough first showed itself, or when it was first observed as a specific disease. Almost all authors agree in this, that the first well- established accounts are derived from Schenck (circa 1650) and Baillou (circa 1600), and refer to epidemics of tussis convulsiva 680 STEFFEN.—WHOOPING-COUGH. in the sixteenth century. All supposed previous descriptions of this disease are far from being characteristic of it, but seem to have been based upon epidemics of bronchitis or influenza. Among the works upon whooping-cough which immediately followT the above, that of Ettmuller (1685) is to be specially men- tioned. The disease seems now to have spread rather rapidly. Moreover, we may judge how considerable was the prevalence of whooping-cough in certain places during the second half of the sixteenth century, from the report that in the year 1580 nine thousand children died from it in Rome. In the course of the eighteenth century it extended over the principal part of Europe, and also over quite a number of coun- tries in other parts of the world, and seems, from its rapid and energetic development, to have had a preference for certain regions. The consequence is that people paid closer attention to this form of disease in various quarters, and in the second half of the century, especially, several works regarding it were pub- lished in Germany, England, and Sweden, e.g., by Alberti (1728), Fried. Hoffmann (1732), Sauvages (1757), N". Rosen von Rosenstein (1768), M. Stoll (1779), Butter (1773), "Willis (1782), McCullen (1784), Fr. C. Meltzer (1790), C. W. Huf eland (1793), Girtanner (1794), C. Sprengel (1794 and 1797), and others. Bier- mer (1. c, p. 535) has compiled a synopsis of the epidemics of whooping-cough which prevailed in the eighteenth centurj^ in Europe and other countries. It seems always to have been assumed that whooping-cough was of a contagious nature. As the ideas of a humoral pathol- ogy were the prevalent ones in the eighteenth century, authors and physicians, with few exceptions, sought for the cause of this disease in disturbances of digestion. These latter, it was sup- posed, exerted an irritating action upon the diaphragm and respiratory organs, and thus caused the attacks of coughing. With the constantly increasing geographical extension of whooping-cough since the beginning of this century, the observa- tions and treatises on it have naturally accumulated. In the first half of this period we find a large number of works published, especially in Germany, England, and France. Among the more important of this date belong, in Germany, Danz (1802), E. Horn HISTORY. 681 (1803), Fr. Jahn (1803), Paldamus (1805), A. Fr. Marcus (1816), J. Frank (1823), Kruckenberg (1824), Faber (1834), Aberle (1843), Canstatt (1847); in England, Okes (1802), Webster (1822), Ham- ilton Roe (1833), Copland (1842), Duncan (1847), Herapath (1849); in France, Gallerand (1812), Guersent (1825), Guibert (1824), Des- ruelles (1827), Blaud (1831), Blache (1833), Trousseau (1843), Barthez and Rilliet (1843). The conviction is constantly gaining ground that whooping-cough has its origin in the nervous system, the respiratory nerves and sympathetic. Some are of opinion that the cause of the seizures is to be sought in the peripheral ramifications, others in the centres of the nervous system. These views, moreover, differ as to whether tussis convulsiva is to be defined as a pure neurosis or as a catarrh of the respiratory organs, combined with an affection of the respiratory nerves. In very recent times, since the middle of this century, a great number of works on whooping-cough have appeared, including in addition many histories of cases. Even now we are met by almost the same theories regarding it as formerly. At the pres- ent time the disease is considered by some authors as a pure neurosis, as it has been already by Copland, Webster, and others, and its origin either transferred to the nervous centres, or ascribed, as it is by Friedleben and others, to the pressure of swollen tracheal or bronchial glands upon the vagus nerve. In opposition to this Broussais1 and Desruelles had already main- tained that whooping-cough was nothing but an inflammation of the mucous membrane of the respiratory organs. The latter author, however, admits that a condition of hyperaemia and irrita- tion of the brain and its membranes is associated with the inflam- mation. Marcus, Blache, Oppolzer, and especially Loschner, are most decidedly committed to defining whooping-cough as a simple bronchitis, which mainly involves the finer bronchioles and the alveoli. They would explain the accesses of coughing as a reflex irritation produced by the decomposed secretion. Beau, comparing these accesses of coughing with those whichi are caused by the entrance of a foreign body into the larynx, felt compelled to assume the existence of an inflammation of 1 Annales de la med. physiolog., 1824, p. 471. 682 STEFFEN. —WHOOPING-COUGH. that part of the mucous membrane of the larynx which lies above the glottis; from this a drop of secretion would some- times fall into the glottis, and occasion these seizures. Some who regard the catarrh of the respiratory organs as the foundation of tussis convulsiva, can find in the paroxysms of coughing nothing which does not belong to them from the location of the trouble. On the other hand, others maintain that a definite specific cause determines this catarrh and the paroxysms, or that the latter are due to a peculiar decomposi- tion of the secretion, which at the same time assumes a con- tagious character. Letzerich has endeavored to show that the explanation of whooping-cough is to be found in the inhalation of a kind of spores, which produce the paroxysms after they have undergone a rapid and considerable increase. Finally, we must consider one more theory which was adopted by famous clinical observers like Canstatt, Lebert and others, although it has now but few adherents. It is that whooping-cough is due to a zymotic affection of the general sys- tem, and that the paroxysms only indicate that the respiratory organs are the part of the body the most involved. Some authors, as Volz,1 J. Frank, and others, classed this so-called general affection among the acute exanthemata, particularly because epidemics of whooping-cough often precede or follow those of measles, or both occur close together in the same place or the same individual. Definition. The essential features of tussis convulsiva, whooping-cough, Keuchhusten, coqueluche, pertosse, kikhosta, etc., further desig- nations of which are to be looked for in Biermer's work, consist in a catarrh of the respiratory organs; not merely of the infra- glottic region of the larynx, of the trachea, bronchi, and their ramifications, but also often, especially in small children, of the nose, and this latter process is indicated by marked parox- ysmal sneezing. The catarrh may attain different degrees of intensity, and be of variable duration. It occurs only through infection, and in fact the entrance of the contagious substance ' Haeser's Arch., Vol. VI., 3. MODE OF OCCURRENCE. 683 is effected by inhalation. The whooping-cough may be con- fined to this catarrh. Should the disease develop to a higher degree, there set in violent convulsive attacks of coughing, with intervals which are free from it. In consequence of the irritation of the branches of the vagus in the respiratory mucous membrane, and especially of the internal branch of the superior laryngeal nerve, by the specific catarrhal secretion of the affected organs, there occurs a spasmodic contraction of the muscles of expiration, and a spasmodic narrowing, sometimes amounting to closure of the glottis. The action of this sort of respiration is manifested by more or less violent ringing coughs following rapidly one after another, and which are generally interrupted by whistling spasmodic inspirations. During the attack the action of the heart is essentially interfered with. With the remission of the spasm some secretion is expectorated from the air-passages, although this is not a necessary feature, and the contents of the stomach also are often vomited. If the disease has been developed up to this stage, as it subsides there follows in every case a period which is characterized by a catarrh only of the respiratory organs, with more or less abundant secre- tion, but without these attacks of spasmodic cough. The whole disease has a duration of several weeks, or even months, and is in itself unaccompanied by fever. Mode of Occurrence and Causation. At the present day whooping-cough occurs everywhere in Europe, and in most countries in other quarters of the world. It has nowhere been possible to prove an independent development of this disease, although it must be said there is no decided evi- dence against the possibility of its originating in this way. On the other hand, the importation of the contagium from without has often been positively determined, especially in sparsely inhabited islands. The disease occurs as an epidemic much more often than sporadically, and in the former case is apt to run a severer course. Climate seems to have no controlling influence on the devel- opment or intensity of the disease, although it does look as if 684 STEFFEN. —WHOOPING-COUGH. the colder, and especially swampy regions were more likely to exercise a harmful influence than those which are warm and dry. The facts cited by Hirsch (II., p. 105) prove how extensive and dangerous may be the spread of such epidemics in a cool climate. According to these, about 72,000 persons, or one- fortieth of the whole number who died, succumbed to whooping- cough in England and Wales in the period from 1848 to 1855. Wilde reports from Ireland that the disease is almost endemic, and ranks fifth in mortality among epidemic diseases. Accord- ing to Rosen von Rosenstein, over 43,000 children died of this disease in Sweden between 1749 and 1764. As many as 5,832 children fell victims to it in the year 1755, while in favorable years the number scarcely reached 2,000. On the other hand, 9,000 children died in the year 1580 in Rome, situated in a warm country, although, to be sure, surrounded by marshes. The seasons, as Hirsch has proved, have no influence on the tendency to the reception of the contagious matter of whooping- cough, or the diffusion of this disease. Earlier observers, not relying, it is true, upon a large number of cases, maintained that a more favorable soil for the development of this disease was furnished in winter and spring,—in the cold and rainy sea- son in the tropics,—especially with sudden and considerable changes in the temperature. Only this, however, appears to be established, that in the winter single cases, whether they be sporadic or belong to an epidemic, have a tendency to run a slower course, because the patients cannot be exposed to mild out-of-door air. According to Hirsch, no differences exist among races and nationalities in respect of liability to the attack or dissemination of whooping-cough. As regards sex, all observers who have a considerable amount of material at command agree that the female is more readily attacked than the male. Bouchut, out of 33 cases, records 12 boys and 21 girls. Aberle, " 356 " " 123 " 223 " Macall, " 307 " " 163 " 143 " Ch. West, " 100 " " 44.7^ " 55.3#" MODE OF OCCURRENCE. 685 With regard to age, the experience of authors is a little at variance. Barthez and Rilliet assign the period from one to five years as that in which they have observed the most cases of tussis convulsiva. They have seen one case in a new-born child whose mother had been attacked with this disease four weeks before her confinement. On the very day after birth violent seizures occurred. This disease is rare up to the end of the first half-year of life, somewhat more frequent from six months up to a year. It is rare from the fifth to the seventh year, and grows constantly less frequent from then up to puberty. According to Wunderlich, the time of life below eight years shows the greatest tendency. Blache had 106 children under eight years of age out of 130. According to Bouchut, a child was infected on the second day of its life, and on the eighth had a well-developed whooping- cough. Biermer observed the majority of those suffering from this disease before the sixth year of life. It seems to occur most frequently in the first two years, though but seldom in the first six months. According to Steiner, children contract the disease most readily between two and seven years. He has even observed cases in children of from two to three weeks, but these are rare, as is the case especially with nurslings. According to West, by far the largest number of cases, 82.9 per cent., fall within the first five years of life. Bednar has observed the disease between the third month and the eighth year of life. Macall found 52 per cent, under two years, 84 per cent, up to four years, 3.25 per cent, over six years, 5.2 per cent. up to two months. My own experience agrees with this as a whole, but I am obliged to make the period in which I have seen the greatest num- ber of cases extend from the first up to the eighth year of life. The nearer children approach to puberty the more rarely does whooping-cough attack them. Still I have observed it in some instances in persons between forty and fifty years of age. Biermer cites cases from Heberden,1 who had seen a woman of 1 Op. Medic. Lips., 1831. 686 STEFFEN.—WHOOPING-COUGH. seventy years and a man of eighty years suffering from it, and from Berger, who had seen it in a woman of fifty-seven. Individual predisposition to be attacked by wdiooping-cough is as much a characteristic of this disease as it is of other infec- tive maladies. It cannot, however, be determined on what this depends, apart from age and sex. It is maintained, to be sure, that delicate, weakly persons who suffer from chronic distur- bances of nutrition have a greater tendency to it than the strong and healthy. I cannot assent to this opinion. I have often in the same family seen delicate anaemic children go through with this disease more easily, and suffer less from it, than strong and full-blooded ones. It seems as if children who are or have been suffering from the acute exanthemata—measles, for example,— show a greater tendency than some others to be attacked by tussis convulsiva. In general, many are attacked by this disease in childhood, adults but seldom, some persons never. In common with the acute exanthemata and most infective diseases, whooping-cough has the peculiarity that persons who have once gone through it acquire a certain immunity from it. It may even be said that a second attack of whooping-cough, when both are reported independently by trustworthy observers, is of vastly rarer occurrence than that persons should be affected a second time with an acute exanthem, such as scarlatina, mea- sles, roseola, or small-pox. There has always been much controversy over the causation of whooping-cough. The view of the humoral pathologists of the eighteenth century which referred the irritation of the dia- phragm and other respiratory muscles, as well as that which determined the paroxysms of cough, to disturbances of diges- tion, may be indulgently set aside. Neither can the assumption that whooping-cough is an inter- nal neurosis be regarded as valid. In regarding the cyanosis and oedema of the face, and the conditions discovered post-mortem, viz., hyperemia of the brain, of its membranes, of the medulla oblongata, and the exudations connected therewith, as causes and not as results of the attacks of coughing, we make the same error as is often made in respect to spasm of the glottis. Even if these conditions have existed previously to the development of MODE OF OCCURRENCE. 687 the whooping-cough, we should still have to regard them as simply associated with it. At the end of the last century and the beginning of this, various authors, especially Huf eland, Jahn, Breschet, and others, in order to give support to the idea of a pure neurosis, maintained that a material lesion, an inflammation of the vagus nerve, lay at the bottom of whooping-cough. This nerve was said to have been found swollen and reddened. More thorough investigations at autopsies have proved this view untenable. With a similar view, Friedleben and others inferred that swelling of the tracheal and bronchial glands, by pressure upon the recurrent nerve, might occasion the seizures of tussis convulsiva. With regard to the possibility of this process I must refer to what I have stated on the subject in the section on Spasm of the Glottis. But, even if we concede its possibility, two things still attract our attention: first, that so many chil- dren exist with considerable swelling of these glands without contracting whooping-cough ; secondly, that the duration of the latter does not always coincide with the duration of the swelling of the glands, but is generally much shorter. The following facts are directly opposed to this view of tussis convulsiva: 1. Its occurrence as an epidemic. Neuroses do not spread in this way. 2. The origin and subsequent diffusion of the disease by infection. This is just as little observed in neu- roses. 3. The absence of a tendency to relapse in whooping- cough, while with neuroses it is well known that such is apt to be the case. Just as little is whooping-cough to be regarded as a zymotic disease of the general s}rstem, in which the exciting cause of the malady is specially localized in the organs of respiration. This idea has been deduced from the observation that this disease, in common with certain infective diseases, attacks the same individ- ual but once; and further, that it seems to show a sort of con- nection with measles, scarlatina, and small-pox, because it has been epidemic at the same time with these diseases, or before or after them. Cases have undoubtedly happened in which, in the same person, the outbreak of whooping-cough has followed eight or ten days after the eruption of measles, which reminds us of the analogous instance of the simultaneous occurrence of 688 STEFFEN.—WHOOPING-COUGH. two acute exanthemata in the same individual, a process which, although rare in recent times, has still been positively estab- lished. Whooping-cough has rarely been observed to develop simultaneously with the prodromata of measles. According to Barthez and Rilliet, this cough does not generally appear until some weeks or months after the subsidence of the exanthem. Faber maintained that tussis convulsiva and measles mutually excluded each other. Equally false with this is the conclusion, to which J. Frank and others have come, that the nature of both processes is the same. Quite apart from the consideration that the essence of these acute exanthemata is widely different from that of whooping- cough, the table prepared by Hirsch also shows that out of 416 epidemics of tussis convulsiva, in only 107 could any coinci- dence whatever with epidemics of these acute exanthemata be proved. The absence of fever and the free intervals argue posi- tively against its zymotic character. A catarrh of the respiratory organs lies at the foundation of whooping-cough. This affects principally the mucous mem- brane of the larynx within the glottis, of the trachea, the bron- chi, and their ramifications, extending sometimes even to the alveoli. In rare cases, especially in small children, the nasal mucous membrane is also involved. This catarrh arises from infection, and consequently it, as well as its secretion, has a specific quality, which may certainly be proved, but cannot at present be more closely defined. The proof of the specific char- acter is furnished by the infection of other individuals, as a result of which the same disease is developed in them. The mode in which the infection takes place is that the contagious substance gains access to the respiratory organs during respira- tion, and there sets up the specific catarrh with its secretion. We do not know of what kind this infectious substance is. It is either simply of a gaseous nature, and is thus inhaled, or there may be very minute particles contained in this gas, which are the proper vehicles of the contagium, or themselves consti- tute it. It is natural that various hypotheses have been broached as to the character of this infectious substance. Let- zerich, especially, has sought to establish by his investigations MODE OF OCCURRENCE. 689 in the year 1870, that whooping-cough originates in a kind of fungi which are taken in during respiration, which increase rapidly, and cause the peculiar symptoms. Attractive as this view appears, it has not yet been well enough established, and has even been disputed by other experimenters of repute. Let the contagium be what it may, it is certain that after it has gained entrance into the air-passages it sets up a catarrh which produces a secretion of specific character. The peculiar- ity of this latter lies not merely in the fact that it contains the infectious matter, but also that this increases with rapidity, so that this increase has a certain duration until such time as it abates, and the contagium is gradually destroyed. If the secre- tion has acquired a character which renders it capable of exer- cising a sufficient degree of irritation upon the catarrhal mucous membrane, the characteristic attacks of coughing are determined as a reflex phenomenon by the excitation of the branches con- cerned of the vagus nerve, or, in the larynx, of the internal twig of the superior laryngeal. The reception of the contagium by other individuals is effected principally by the stay of such persons in an atmos- phere impregnated with the infectious substance exhaled by patients. Such an atmosphere is found in a room in which patients are, or have been shortly before, and if they are in the open air, then in their neighborhood. Since, however, the con- tagium may not only be exhaled in a gaseous form, but is also contained in the secretion of the air-passages, we may assume that the fresh sputa of a patient with wdiooping-cough are capa- ble of proving infectious from the development of gases. By some authors this quality is even ascribed to the dried expecto- ration. We should therefore avoid using for healthy persons handkerchiefs, towels, etc., which have been used about chil- dren suffering with whooping-cough. It seems to me exceed- ingly doubtful, if it be possible, for healthy persons, without being themselves infected, to convey to others any substance clinging to their clothes, so that the latter shall be attacked with whooping-cough. I at least have never observed such a train of events. Some authors have maintained, especially in recent times VOL. VI.—44 690 STEFFEN.—WHOOPING-COUGH. Oppolzer and Loschner, that there is no other process at the bottom of attacks of whooping-cough but a simple bronchitis, which extends into the finest subdivisions, often even into the alveoli. They claim that the secretion adhering in these places, and stagnating there, undergoes a decomposition, and on the one hand occasions the attacks of cough by the reflex irritation it develops. On the other hand, through the secretion so consti- tuted, the possibility is "acquired of its conveying a similar process to other individuals, in analogy with the communica- bility of acute catarrhs especially, which by means of their secretion are capable of setting up the same process in other persons. In opposition to this view it is to be said that a simple bronchitis never sets in with the characteristic symptoms of whooping-cough ; that it never shows the peculiar course of the latter; that it is not contagious in the same sense as this, and that it may have quite frequent relapses, to which whooping- cough scarcely ever shows a tendency. Nor is it at all necessary that the bronchial catarrh in whooping-cough should extend into the bronchioles and alveoli, any more than that a certain amount of secretion must be present to occasion the attacks of coughing. Very respectable attacks of coughing are often observed in which hardly anything is expectorated. If they were excited by a con- siderable amount of secretion, they could not cease until this was removed. Gendrin and Beau believed that it should be assumed, in ana- logy with the seizures of cough wThich take place when a foreign body enters the larynx, that a similar condition lies at the root of the attacks in tussis convulsiva. They proposed the hypothe- sis that in this disease a catarrhal inflammation of the entrance and upper portion of the larynx was present. If any of the secretion fell from here into the glottis, the attacks in question would be set up. It does not agree with this that at the height of the process patients are apt to cough harder and more fre- quently at night than by day, although the horizontal posture in the night ought to diminish the tendency of the secretion to flow into the glottis, and the erect position in the day to increase it. The post-mortem appearances may be delusive in this respect, because the hypersemia and swelling of the mucous SYMPTOMS AND COURSE. 691 membrane may have diminished after death. Now although Beau is inclined to sustain his theory by laryngoscopic inves- tigations, similar investigations of others, particularly of Rehn, decidedly controvert it. This observer, in fact, found in adults the supra-glottic region normal, while, on the other hand, the infra-glottic region and the upper part of the trachea were red- dened and swollen. Among the predisposing causes, which may determine the attacks when whooping-cough is present, is primarily to be men- tioned a sudden change of temperature, especially passing from warm to cold. In addition to this the purity of the air has an important influence. Hauke has proved by experiment that contamination of the air with carbonic acid is apt to augment the intensity and frequency of the seizures. This may be the explanation of the fact that the disease is wont to attain a higher degree at night, as well as that patients have a greater tendency to these attacks if they are in rooms, whether large or small, which are crowded with people. A brisk wrind or air, rendered impure from dust, is likewise injurious. Besides this the attacks are provoked or intensified by all active movements of the larynx, such as continued speaking, crying, etc., as well as by taking food or drink, especially if anything should find its way into the larynx. Rapid movements of the body and mental emotions, as well as external pressure on the larynx, smoking, and the taking of spirituous drinks, may act as pre- disposing causes of the attacks. Finally, it cannot be denied, that in children even the regimen may at times contribute towards allowing the more rapid development of the seizures. Symptoms and Course. Simple whooping-cough manifests itself in the form of parox- ysms which are followed by intervals during which the patient is free from cough. These seizures vary according to age, pre- disposition, and the intensity of the infection. For the sake of greater simplicity I follow the ordinary division of this process into three stages: 1. The stadium pro- dromorum, which, after the infection has been received, is mani- 692 STEFFEN.—WHOOPING-COUGn. fested only by the symptoms of a catarrh of the air-passages, with more or less violent cough. 2. The so-called convulsive stage, which sets in with the characteristic attacks. 3. The final stage of a catarrh of the respiratory organs, with abundant secretion, but without characteristic attacks of cough. Strictly speaking, this division does not properly exist. The separate stages often pass so imperceptibly from one into another that the dividing lines cannot be positively drawn. For the stadium prodromorum may be so briefly and imperfectly developed as to be overlooked. In rare cases it seems possible that it may be wholly absent. Finally, the first stage may run its course, and the disease terminate without the second stage having developed. The chief characteristic, then, of the first stage is a catarrhal affection of the respiratory organs. In the majority of cases the larynx is found to be attacked from the very outset, and thence the process extends downwards to the trachea, the bronchi, and their larger branches. Occasionally the disease begins as a catarrh of the nasal mucous membrane, with smart sneezing, which is sometimes quite frequently repeated in a short space of time, and there is also considerable discharge of a muco-purulent secretion. More often the mucous membrane of the pharynx is found to be simultaneously attacked, even at the beginning. This stage sets in suddenly without premonitory signs. Chil- dren, who have been perfectly healthy up to this time, begin to cough as soon as the larynx is affected. The cough generally exhibits no special characteristics ; it is teasing and urgent, and accompanied by little or no expectoration. In certain cases, particularly if this stage is drawing to a close, and is about to pass into the spasmodic, it is found that the paroxysms are more violent, and the individual coughs are repeated more frequently, and follow more closely one upon the other. Trousseau main- tains that they may often be repeated forty or fifty times in a minute, and that this violence of the cough may show itself very obstinately through a series of days. In rare cases this stage begins, especially at night, with an attack of catarrhal inflamma- tion of the mucous membrane of the larynx, with acute swelling of the tissues, and a cough which, in consequence of the exist- SYMPTOMS AND COURSE. 693 ing narrowing of the glottis, presents, both in the sound of the expirations, and in the spasmodic, whistling inspiration by which they are interrupted, the most marked resemblance to that of laryngeal croup. By the next morning these symptoms have disappeared, and the catarrhal stage of the whooping- cough has begun. We sometimes see this stage run its course without fever, while sometimes there is a moderate degree of it, as in many acute and wide-spread catarrhs. The setting in of the fever is not indicated by an initial chill. Moreover the fever is apt to have no regular course, but is subject to oscillations, which are likewise quite irregular, and are manifested by an increase of the pyrexia after slight chilliness, alternating with some heat. The children look pale and weak, are fretful, with little appetite, and increased thirst, and sleep uneasily; their heads are somewhat affected, and the conjunctivae moderately injected. Nothing can be gathered from these symptoms which can be regarded as premonitory of whooping-cough. They are precisely X like those of any catarrhal inflammation of the respiratory organs. In rare cases this stage is entirely absent in nurslings, or is limited to one or two days. But even here a duration of as much as one or two wTeeks has been observed. Berger has esti- mated this stage as averaging from eight to fourteen days, Lom- bard from four to six wreeks. Wunderlich assigns from half a week to six weeks; West, from two to thirty-five days. From these notes it is perceived how variable the duration of this stage is. In young children it is apt to be the shortest, and to last longer in older ones. On the whole, however, this difference depends upon the predisposition, and the violence of the infec- tion. In other respects there is no doubt that in very many cases it may be difficult, or even impossible, to determine with certainty the beginning of this stage, or its passage into the second. The whole disease may come to an end with the expiration of this stage, if the predisposition to infection has been too slight, or the contagium not sufficient in intensity and amount to pro- duce the spasmodic stage. In considerable epidemics this course 694 STEFFEN. —WHOOPING-COUGH. of events is quite often observed, most frequently among chil- dren at the breast. In the majority of cases the first stage is followed by the spas- modic stage, either gradually and insensibly, or sometimes sud- denly. The febrile symptoms which had accompanied the first stage diminish, and there are intervals perfectly free from fever. The attacks of coughing grow by degrees more violent and spas- modic. For some ten minutes before the onset of the attack the children become restless and anxious, call upon their attendants, run to them and seize them as if they were seeking help ; older children run to the spittoon or some other vessel, so as to deposit in it, when the expected seizure comes, the sputa, and ultimately the matters vomited. The attack is sometimes preceded for some minutes by nausea. The feeling of anxiety is portrayed in the children's countenances. Older children and adults assert that sensations of tickling or scratching, or of the presence of a foreign body in the larynx, occur as premonitions of the attack. Some- times, too, there is a sensation as if the larynx were being com- pressed, and as if a certain degree of insufficiency of breathing were caused thereby. This feeling of constriction of the air-pas- sages often extends down the trachea. It is not unusual for persons standing near to hear coarse rales in the trachea and bronchi of the patient before the seizure, and these may be even more clearly perceived during sleep. From the latter circumstances the theory has been deduced that the attacks of cough are occasioned by the specific secretion, which, being brought up from the deeper air-passages irritates the portion of the larynx situated below the glottis, already the seat of catarrh, and sensitive from it. As a reason for this it has been alleged that after the expectoration of the secretion the attack stops. It cannot be denied that this theory sounds very plausible, and may certainly serve as a partial explanation of the attacks. Still, it is to be borne in mind that there are attacks without anything being expectorated, and that the irritation of the bronchial mucous membrane may, in itself alone, suffice to excite decided coughing. One has only to call to mind the attacks of cough produced by a foreign body which has entered some ramification of the bronchi. SYMPTOMS AND COURSE. 695 The attack begins with spasmodic expirations following one after another at brief intervals, and which may be of variable intensity, and the sound of which is dependent upon the degree of narrowing of the glottis existing at the time. The latter may be very slight, and then the resonant sound of the expiration presents nothing striking, while if the constriction is considera- ble this sound may be similar to that in croup. In the slighter cases the inspiration which is made between these expirations has no special characteristic, and is scarcely audible. The more violent the attack the more rapidly do the expirations follow; the more the glottis is narrowed the more will the inspiration be spasmodic, long-drawn, and accompanied by a whistling sound, the whoop. In the shorter attacks this inspiration is heard but once, while in those which are more violent and long- continued it may be perceived several times, so that an inspi- ration follows every time upon a certain number of expira- tions, and the attack is finally brought to an end by expirations. When this happens a viscid, tenacious secretion is generally expectorated from the air-passages. If the attacks are rather violent the contents of the stomach are vomited at the same time, especially just after taking food. Just before the beginning of an attack the respiration and action of the heart are quickened. During the attack speech is interfered with ; only a few almost inaudible words can be forced out. The expression of the patients indicates a greater or less insufficiency of breathing. Older children brace themselves with their arms so as to facilitate inspiration. Tears flow from the eyes, the nostrils move convulsively. The face, which at the be- ginning may be moderately suffused, becomes livid, and in vio- lent and long-continued attacks may attain to quite a high degree of cyanosis. At the same time it is bloated from the hyperaemia due to interference with the circulation, and this con- dition is apt to last during this stage, and even longer, so that in some cases the expression of the child seems completely altered. The extremities become cool; sometimes a cold sweat breaks out. Moderate hemorrhages from the nose and mouth are not unusual during the attack. Often, too, the faeces and urine are expelled involuntarily. The younger the children the more easily are 696 STEFFEN.—WHOOPING-COUGH. they stupefied by any considerable passive congestion of the brain during the attack, and often remain in this condition for a short time afterwards. Examinations of the larynx during an attack are not practi- cable either with the laryngoscope or with the stethoscope. Examination of the lungs during the spasmodic expirations, in the course of which some air is continually driven out, and that contained in the respiratory organs compressed, gives a deadened and shorter percussion note. Auscultation in the main furnishes only a negative result. The spasmodic inspiration is distinctly audible with the stethoscope, especially the older the children are, and percussion again reveals the normal resonance of the lungs. As a matter of course, while these processes are going on, the lower borders, as well as those edges of the lungs which partly cover the heart, suffer the displacement due to the exist- ing state of affairs. During the attack the action of the heart is essentially im- peded by the passive congestion which has occurred, and partly on this account, and partly also, it may be, from the notable irritation set up in the vagus nerve, the heart's action may cease altogether momentarily. Moreover, we must assume that a tran- sient dilatation of the heart is produced by the passive conges- tion, and that this has an injurious effect upon its action. After the attack is over, the relations of the respiration and circulation gradually become normal again. The patients are for a short time languid, depressed, and irritable, preferring a re- cumbent position until the effects, with perhaps the exception of the swelling of the face, disappear. If the attacks are repeated, at short intervals, and especially if they are of an aggravated character, the patients may not be able to recover themselves between times. They remain depressed and apathetic, prefer to lie down constantly, their strength diminishes, they grow thin, especially when the attacks are accompanied by frequent vomit- ing of what has been eaten. It happens not infrequently that a second attack follows immediately upon the first, if no sputum has been expelled, and it is then generally expectorated with the second. This process likewise argues against the absolute valid- ity of the theory that the attacks are caused the moment any of SYMPTOMS AND COURSE. 697 the bronchial secretion gets into the infra-glottic region. In the cases under consideration this must be present in the deeper por- tions of the air-passages, for otherwise it would inevitably have been discharged with any one of the spasmodic expirations. Physical examination instituted in the intervals always shows the symptoms of catarrhal tracheitis and bronchitis, and, according to whether the process has or has not extended to the finer bronchial ramifications, it exhibits the peculiar features belonging to them. The condition of the heart is found normal. The duration of the attacks is from a few seconds to several minutes. Their number in the twenty-four hours may be small, or may increase to from sixty to eighty. Macall claims to have observed in a child, eight months old, the enormous number of 140. They are apt to be more frequent and violent at night than in the daytime ; so that, as a rule, it may be assumed that with the remission of the nocturnal attacks this stage is tending to its close. The more violent the attacks are, the more numerous and the more marked are the manifestations to which they give rise. These latter are mainly dependent upon disturbances of the circu- lation and respiration. To the former belong the rupture of small vessels and the resulting hemorrhages. Hemorrhages from the nose and mouth are nothing unusual. Sometimes, however, they are profuse, and accompany almost every attack for days and weeks, so that the life of the child may be endangered from the loss of strength. The hemorrhages from the mouth may originate in the mucous membrane of the buccal cavity and pharynx ; they may also come from the larynx. Hemorrhages from the more deeply situated air-passages, viz., apoplexies of the lungs, have not as yet been observed during life. Hemor- rhages into the conjunctiva, sometimes quite extensive, are not seldom observed. Generally they involve both eyes, and in like manner the extravasation of blood into the surrounding tissues, which is often quite considerable, is apt to be on both sides. Trousseau has seen blood escape from the conjunctiva and mix with the tears. Ecchymoses of the cheeks and throat are less common, and ordinarily of small compass. Hemorrhages from the ears, with perforation of the drumhead, have been several 698 STEFFEN.—WHOOPING-COUGH. times observed. Roger in such a case has seen the blood spirt out. Effusions of blood into the brain, the meninges, and be- tween tliese are rare. In consequence of the passive congestion the neck may be swollen during the attack, and its veins filled to distention. There may occur oedema of the brain, or transudations into the ventricles and between the membranes. The case observed by Sebregondi, in which a girl of six years is said to have become blind with every attack, must in like manner be referred to the blood stasis. A year ago I treated a girl of eight years who saw indistinctly during the attack, but also lost some of her sharp- ness of sight in the intervals, as long as the spasmodic stage lasted. The more violent the expirations are in the attack, and the more rapidly they follow one another, so much the more posi- tively is spasm of the glottis developed with narrowing of its chink. Since enough air cannot escape through the latter, in spite of the violent expirations, what remains behind is com- pressed to the utmost by the muscles which preside over respi- ration, and it may even result in injury to the vesicles of the lungs. From their being so distended by the air spasmodically forced into them, emphysema results, which, as a rule, is apt to involve only the superficies of the lungs or certain peripheral sections, and then passes off without any symptoms. If the whooping-cough does not last too long, and the elasticity of the alveoli is retained, this condition may again pass into a per- fectly normal one on the subsidence of the attacks. Under opposite conditions it may continue, and if the attacks attain a very high degree, it may increase, by rupture of the alveoli, to interstitial and mediastinal emphysema. Perforation of the pleura with subpleural emphysema, and the development of pneumothorax are exceedingly rare, and, in fact, as a rule, fatal, because the fits of coughing do not allow of reabsorption of the air which has escaped, and are constantly forcing it back anew, so that the seat of rupture cannot close. More frequently, after the previous occurrence of mediastinal emphysema, the development of a general emphysema has been observed, which has involved at least the larger part of the surface of the body. SYMPTOMS AND COURSE. 699 Roger, Blache, Hervieux, J. Frank, Gelmo, and others have published a number of such cases. If the point of rupture of the alveoli closes, reabsorption of the air and complete recovery may ensue. If whooping-cough is severe, we shall not fail to find in the majority of cases an ulcer on one or both sides of the fraenulum linguae, less often on the upper surface of the tongue. These ulcers are shallow, with somewhat elevated edges, which, as well as the base, are of a grayish-yellow color. They depend upon the fact that during the attack the tongue is wounded by being thrust between the teeth at a spot where they are either very much inclined or very prominent. The ulcer disappears of itself, with the subsidence of the spasmodic stage. The first descriptions of this ulcer come from about 1840. In attacks of a high degree of severity the increase of struma has been observed. In like manner the development of herniae and prolapsus ani are met with, or the increase of these condi- tions, if they were already present. Biermer quotes a case from Schott' in which hydrorrhoea was established from rupture of the fcetal membranes during whooping-cough. If the spasmodic stage runs an uncomplicated course, it usually gives rise to no serious apprehensions of any kind. Still it has been observed that in excitable persons the attacks have been the source of severe headaches, which also continued in the free intervals, and sometimes appeared to leave the issue of the disease in doubt. I have seen cases in which the head- aches were constant during the whole duration of this stage. Moreover, there not infrequently occurs a morbidly increased irritability of the brain. This is characterized in its least degree by great sulkiness, which may increase to perfect indifference. In a more advanced degree, especially in connection with pro- fuse hemorrhages, frequent vomiting and loss of appetite, deli- rium may set in, which is dependent upon the inanition of the body and the deficient nutrition of the brain resulting from it. In its highest development Ferber has observed acute mental aberrations at the acme of the whooping-cough. Wiirttemberger Correspondenz-Blatt, Vol. IX., No. 38. 700 STEFFEN.—WHOOPING-COUGH. As a result of profuse hemorrhages, loss of appetite, and dis- turbances of nutrition, after frequent vomiting, a degree of ma- rasmus may be gradually established which may be alarming and fatal. In very rare cases children are seen to succumb suddenly and unexpectedly during a coughing fit. This accident generally occurs to children in the first or second year of life. Their sud- den death may be attributed to various causes. The spasm of the glottis which has taken place may reach so high a degree as to occasion complete persistent closure of the glottis and suf- focation. Death may also result from effusion of blood into the brain, or from considerable transudation into the brain and its ventricles. Besides this, it may be the consequence of paralysis of the heart which may develop after a momentary stoppage of it. Finally, there is the possibility that the rapid development of a diffuse pneumothorax may suddenly lead to a fatal ter- mination. Authors are divided in opinion as to the duration of this spasmodic stage. Gerhardt fixes it at from twro to ten weeks, Steiner at from three to eight weeks. Biermer assigns from four to five weeks as the medium duration, but has also seen this stage last but two weeks, and, on the other hand, several months. According to Barthez and Rilliet it varies between fifteen and sixty-five days. It is difficult to determine the duration of this stage, as it is not always possible to fix its limits exactly. So much as this, however, is certain, that the longer it lasts the more feeble and infrequent do the attacks gradually become, and that when it lasts a long time the attacks are not apt to be either numerous or very severe. If the patient has passed safely through the spasmodic stage, there always follows a so-called stadium decrementi, into which the former gradually merges. The attacks lose their violence and become less frequent, and this is particularly noticeable during the night. The spasmodic inspiration disappears entirely, and the cough assumes the char- acter of that in a simple catarrh of the air-passages. The expi- rations are no longer so violent and spasmodic, and the pauses between them become longer. The feeling as if something were obstructing the breathing no longer precedes the cough. The COMPLICATIONS. 701 secretion of the air-passages is now expelled by the cough, and its character has undergone a change ; it is somewhat thick, yellowish, or greenish, and consists of mucus and pus-corpuscles. The vomiting and the disturbances of the circulation, which were present during the attack, have now ceased. The blood effused into the mucous membrane or the integument is reab- sorbed. The physical examination of the organs of respiration indicates the symptoms of a simple catarrhal affection merely. The appetite, if previously diminished, now speedily returns, and with the disappearance of the cough and expectoration the child recovers its strength in a longer or shorter time, if any adequate power for reaction is present. Still, children even in this stage have been seen to succumb to marasmus. It sometimes happens that patients are believed to have a return of all their symptoms when the stadium decrementi has already been reached. After certain exciting causes the attacks of spasmodic cough are suddenly observed to recur. Still, this stage of relapse is not apt to last long. The period occupied by the third stage is variable. In the most favorable case it may last only a few days, but it may also last for weeks. In many children who have had whoop- ing-cough there may remain for years a tendency to this spas- modic character, even though the cough proceeds from a simple catarrh. The picture of whooping-cough, as here presented, is that of the disease as observed in childhood. When children grow older, that is, after the tenth or twelfth year, and especially in adults, the attacks of cough gradually lose their violence, and the respiratory and circulatory symptoms that follow are less actively developed. The wrhole duration of whooping-cough, which in children may extend over some months, shows itself in adults decidedly shorter. Complications. There are certainly few diseases which may not complicate whooping-cough. Among the most frequent complications are to be reck- 702 STEFFEN.—WHOOPING-COUGH. oned other diseases of the respiratory organs. Among 307 cases of whooping-cough, Macall found eighty-one complicated with other diseases of the air-passages. In very rare cases croupous laryngitis has made its appear- ance in the course of the disease, and almost always with a fatal issue. In Biermer's case the whooping-cough attacks remitted on the setting-in of the croup. Blache, Gauster, and some others have observed this complication. Barthez has seen oedema glot- tidis with a fatal result occur in a girl of four and a half years, who had suffered from whooping-cough for three months. Tra- cheotomy was performed in vain.l A similar case was observed by Benoit. I have once seen typical tonsillitis accompany the outbreak of whooping-cough. In the majority of cases the bronchitis which accompanies tussis convulsiva remains limited to the larger divisions of the bronchi. If it also attacks the bronchioles and alveoli, the seizures are apt to diminish in intensity, or to become less fre- quent. The indications of fever vary; a moderate degree of cyanosis is persistent, but now and then increases without attacks of cough. The variable degree of respiratory insufficiency which is present, depends upon the extent and intensity of the capillary bronchitis, and is sometimes temporarily relieved by a free expectoration of muco-purulent masses, vomiting sometimes occurring in connection with it. The children are very restless, throw themselves about, are fretful, and the appetite diminishes, while on the other hand there is great thirst. Sometimes they are afflicted with intercurrent diarrhcea, and I have also observed profuse sweats. In higher degrees of the affection children are seen to be apathetic in consequence of the stasis of blood in the brain, and its being overcharged with carbonic acid; they take no interest in anything, and rarely make any response if they are addressed or touched. Sometimes they are so stupefied that for hours they cannot be aroused, and their faeces and urine are passed unconsciously. 1 Journal fiir Kinderkrankheiten, 1869, I., p. 221. COMPLICATIONS. 703 Physical examination of the chest reveals labored respiration, bulging forward of the upper portions of the thorax, and below, the peripneumonic furrow (Trousseau); on auscultation, fine, partly sonorous rales in the regions affected by capillary bron- chitis. Sometimes the process has been observed to begin in certain places, diminish, and then involve others. This complication is of a very serious nature, the more so if the process is widely diffused. The majority of those affected in this way succumb to it, rarely suddenly, but only after the expiration of a week or weeks. If the disease passes into con- valescence, the affection of the bronchioles and alveoli first diminishes ; that of the larger branches may last still longer, so that a long time elapses before the patients completely recover. Whooping-cough is found to be complicated with pneumonia just about as often as with capillary bronchitis, especially as the pneumonia develops upon the bronchitis as a foundation. Dif- fuse pneumonias, with exudation into the alveoli and bronchi- oles, are very seldom found. On the other hand, the inflamma- tion of the alveoli and bronchioles passes over to the neighboring tissues, and forms circumscribed pneumonic foci, which extend from one to another if they are situated close together, and if they are present in large numbers may produce consolidation of considerable sections of a lobe, or of a whole lobe. The younger the children are, the more likely is this process to take place under the form of the well-known stripe-pneumonia,1 in the posterior portions of the lungs. At times the lower lobe only is affected, at others the process reaches from the base to the apex. It may be found upon one or both sides ; in the latter case either simultaneously or one side following the other. 1 I have used this term, "stripe-pneumonia," as a translation of our author's word " Streifenpneumonie," which, so far as I have been able to learn, has yet found no recognized English equivalent. In the Jahrb. fiir Kinderheilk., VIII., 3, p. 255, 1875, Steffen thus defines the condition referred to. '' An inflammatory consolidation of the lung tissue in the form of a strip found on one or both sides, at the posterior portion of the lung's, which extends in width from the vertebral column to the angle of the ribs, and in length may include either the whole height of both lungs from base to apex, or merely a single lung or lobe." It is always a secondary affection or complication of some other disease, and occurs in connection with hypostatic congestion, atelectasis, or bronchitis.—Translator's Note. 704 STEFFEN.—WHOOPING-COUGH. The functional symptoms are similar to those of capillary bronchitis, especially as the latter disease is associated with the pneumonia. If neither process, however, is very extensive, the symptoms are apt not to be so severe as in general bronchitis without pneumonia. The respiratory insufficiency and cyanosis are not so noticeable, and even, if the children are apathetic in the higher degrees of the disease, the sensorium is not apt to be affected to any considerable extent. The conditions found on physical examination in general or in circumscribed pneumonia are such as are well known, and are to be found in the sections treating of these forms of disease. All painstaking observers agree that the complication of whooping-cough with pneumonia is just as dangerous as with general capillary bronchitis. About two-thirds of those affected with it die, and this takes place the more quickly the younger the children are. Generally, the majority of fatal cases is to be ascribed to this complication. Out of twenty-seven fatal cases Charles West observed thirteen complicated with capillary bron- chitis and pneumonia. Macall ascribes two-thirds of the fatal cases in whooping-cough to this complication. Still the course of the pneumonia is apt to be much more prolonged than that of the bronchitis. Suddenly fatal cases do not occur in this dis- ease. It may, however, last for weeks or months, whether its termination be favorable, or the reverse. A complete recovery, in which no traces of the affection are left behind, is, to be sure, exceedingly rare. Usually there remains a partial emphysema, due in part to the whooping-cough, and in part to the inflamma- tory condensation of the lung. Moreover, there remains in those regions which were attacked by the inflammation a retraction of the interstitial tissue, and partly from this, and partly from the same law under which the emphysema develops in whooping- cough, there remain partial dilatations of the bronchi with per- sistent catarrhal symptoms. If the pneumonic foci fall into the retrogressive course of caseous formation and degeneration, the patients sink with the symptoms of pulmonary phthisis. Not infrequently atelectasis is developed in the course of the capillary bronchitis of whooping-cough, particularly in younger children, in isolated points, or even involving more considerable COMPLICATIONS. 705 areas. The reason is found in the plugging of the bronchioles by secretion that cannot be expelled from them,—a result brought about by the absorption of the air contained in the affected alveoli followed by their collapse. The functional and physical symptoms render it difficult to distinguish this process from pneumonia, especially as it is generally allied with pro- cesses which are accompanied with fever. With younger chil- dren it has this additional resemblance to pneumonia, that it not seldom occurs in the stripe form in the posterior parts of the lungs. If the obstacle to the entrance of air into the alveoli is not removed, circumscribed pneumonia develops itself at tliese places. A sudden occurrence of consolidation in the lungs would rather lead us to infer atelectasis than pneumonia. In many quarters, and with justice, stress is laid upon the frequent occurrence of pulmonary phthisis after whooping- cough. The connection may be of various kinds: in the first place, the degeneration of cheesy pneumonic foci may in itself cause phthisis; then again, we may have to do with a sec- ondary development of acute or chronic tuberculosis in the lungs alone, or in other organs also. This tuberculosis may originate in the pneumonic foci indicated, or also in tracheal and bronchial glands which had entered upon the condition of hyperplasia and cheesy transformation even before the begin- ning of the whooping-cough. This affection of the lymphatic glands is, however, in many cases, also primarily the result of a long-continued or very violent bronchitis or pneumonia. For the development of tuberculosis may often not occur till long after these inflammations have run their course, and that too even favorably. It is well known that pulmonary phthisis occurs after chronic tuberculosis only through the secondary development of an insidious pneumonia. Finalby, it is plain that chronic tuberculosis and pneumonia, when already present, may be brought into a condition of greater activity by whoop- ing-cough. It is known that pneumonia seldom runs its course without pleurisy ; yet in this connection it is apt to be more of a paren- chymatous nature and to furnish only a little free exudation. Pleurisy without pneumonia has scarcely been observed in VOL. VI.— 45 706 STEFFEN.—WHOOPING-COUGH. whooping-cough. In light cases whooping-cough may run its course without spasm of the glottis. In more severe cases this is not absent, and in intense cases the two keep pace with one another. The spasm may set in with such violence and per- sistency as to result in actual stupor, or sudden death from suffocation. As a rather infrequent complication on the part of the ner- vous centres, are to be mentioned slight convulsive movements, at the height of the attack, in various parts of the body, espe- cially the muscles of the face ; spasmodic movements of the eye- balls are also noticed. In a boy nine years old I saw strabismus internus of the right eye occur during violent attacks, while the left eye was retained in the normal direction by tonic spasm. They are partly the result of the essentially violent excitations of the nervous system, partly of the stasis of blood in the brain and spinal cord. In coughing attacks of the greatest severity they sometimes amount to general convulsions, which, in the majority of instances, prove fatal the first time, or after some repetitions. The intervals which follow are not, as a rule, com- plete, but are marked by slight partial convulsions. West main- tains that this complication furnishes by no means a rare cause among the fatal cases after whooping-cough. Macall estimates them at one-sixth of all the fatal issues. If the children with- stand these attacks, there remains for a long time a morbidly increased irritability of the nervous system. In extremely rare cases, always as a result of centres of disease in the brain, epi- lepsy and chorea have been seen to follow. Rilliet reports the cure of two cases in girls of five and six years old. Ozanam has seen but one child restored to health after convulsions. The complication of pneumonia with acute meningitis or acute miliary tuberculosis of the pia mater, and the results of these diseases, have been observed only in the most isolated instances. Endocarditis and pericarditis are exceedingly rare in whoop- ing-cough. Deafness or hardness of hearing is not an infrequent result of Hemorrhages into the organ of hearing, or of long-continued catarrh of the tubes or tympanum, or of purulent inflammation COMPLICATIONS. 707 of this cavity with perforation of the drum-head and chronic otorrhoea. Among the very frequent accompaniments of whooping- cough, especially if vomiting often occurs with the attacks, be- long want of appetite, impairment of digestion, and catarrh of the mucous membrane of the stomach and intestine. This is a disagreeable addition, particularly in cases where the children are delicate, because the diminished supply of nourishment on the one hand, and on the other the oft-recurring attacks of diarrhoea, may contribute essentially to wear out the strength. Heyfelder has seen cholera as a fatal complication. I have found swelling of the liver in whooping-cough only when pronounced rachitis was present at the same time. The autopsies demonstrated the presence of increased accumulation of fat in the liver cells. At the time of violent seizures, or shortly after them, accord- ing to my observation, albumen may be contained in the urine. Investigations are wanting as to whether admixtures of blood are also present in it. The passive congestion, which is produced in the body by violent attacks of whooping-cough, and often by affections of the lungs also occurring at the same time, may, in connection with increasing marasmus, lead to dropsical troubles which are calcu- lated to hasten the fatal issue. Sometimes these exudations are only partial, in the face and upper extremities, but as they increase the cavities of the body also do not escape. If the strength has been impaired by chronic lesions of nutri- tion, such as rachitis or scrofula, and the foundation thereby laid for spasm of the glottis and for functional or organic dis- turbances of the lungs, there is likely to be a more severe devel- opment of the whooping-cough, and the way is also paved for the diseases I have described as sequelae. I have once seen whooping-cough develop in a girl three years old during convalescence from typhoid fever. The attacks were violent, capillary bronchitis and circumscribed pneumonia set in, and the issue was fatal. Whooping-cough is not infrequently found to be complicated with the acute exanthemata, measles, scarlatina, and small-pox. 708 STEFFEN.—WHOOPING-COUGH. The first is the most frequent. This exanthem has been seen alike to precede, to follow, to develop at the same time with the whooping-cough, or in the middle of its course. The course of the exanthemata is not thus essentially modified, although in many cases where they are associated with whooping-cough, the latter is found to undergo a considerable diminution in respect to the intensity and frequency of its attacks ; it may even dis- appear entirely, in analogy with our experience as to a general outbreak of chronic eruptions of the skin during the subsidence of tussis convulsiva. In the majority of cases whooping-cough follows upon the subsidence of the acute exanthemata, or is developed in the last stage of them. It seems as if children who were ill with the latter, or who have suffered from them, were specially disposed to be attacked by the former. This may not appear strange if we bethink ourselves that the contagium of these exanthemata likewise enters through the respiratory organs, and that, there- fore, in such cases the infectious matter of whooping-cough finds a favorable soil for its reception in the morbidly irritated and hyperaemic mucous membrane. Measles forms a specially unfavorable complication While this disease is subsiding, or perhaps even after it has run its course, a capillary bronchitis or a pneumonia is very likely to become developed. Now whooping-cough, coming on in a per- son who is convalescing from such a pulmonary affection, falls upon respiratory organs which have not yet returned to their normal condition. Besides this, too, it is certain that whooping- cough, wrhich has developed in the course of measles, shows a greater tendency than in any other complication to set up a capillary bronchitis or a pneumonia, and in consequence of it to end fatally. It has been maintained by many that if a febrile disease is associated with whooping-cough, the latter loses somewhat of the intensity and frequency of its seizures, and sometimes disappears altogether. Others declare that they have observed the oppo- site. Both sides are right; both conditions have been observed. Especially is it the rule, that on the occurrence of capillary bronchitis or pneumonia the attacks remit, and become less and PATHOLOGICAL ANATOM Y. 709 less marked. I have had an opportunity of making the following observation with regard to a complication with varioloid. A girl of six years came under treatment on December 24th, 1870. She had suffered for a short time from tussis convulsiva and bronchitis, with intercurrent albuminuria. On January 11th, aphthous stomatitis. On January 16th, an erup- tion of varioloid, with diphtheria on the tongue on the following day. On the 23d, decided diminution of the fever. As early as January 19th the attacks of whooping-cough were less in number and violence. On the 26th the number increased again, to sink on the 29th, remaining stationary then for a time at a lower figure, and then entirely disappearing. The child was completely restored to health. Complications with acute pemphigus are very rare. I have treated in my hospital two such cases with several successive outbreaks of the eruption. They were in two boys of fourteen and fifteen months. Pathological Anatomy. The results of pathological anatomy in regard to whooping- cough are rather negative. The constant occurrence, as laid down by Beau and Gendrin, of catarrhal inflammation at the entrance of the larynx and in the supraglottic region has been proved to be erroneous. On the contrary, in the majority of cases, as it appears, a catarrhal inflammation is found in the infraglottic region. In one case I have seen the mucous mem- brane of the epiglottis and arytenoid cartilages thickened but pale. Breschet and Autenrieth1 maintained that the vagus nerve was reddened and inflamed in whooping-cough. The investiga- tions of Krukenberg, Guersent, Constant, and others have proved the contrary. In every case the presence of a catarrhal inflammation of the air-passages can be established. The mucous membrane of the nose and pharynx is less often attacked. On the other hand, the signs of a catarrhal inflammation from the glottis downwards are present in the majority of cases. Still this is not always the rule. The process often even begins in the large bronchi; farther up, the mucous membrane is pale and not swollen. I have once, in a girl of a year and nine months, seen several shallow ulcera- 1 Tiibinger Blatter, Vol. I., p. 23, 1815. 710 STEFFEN.—WHOOPING-COUGH. tions of small circumference in the reddened and swollen mucous membrane of the trachea. The mucous membrane of the bronchi and their ramifications is swollen, either pale or deep red, and more or less covered with tenacious muco-purulent masses. The calibre of the larger air-passages is often filled with these masses, which have acquired a frothy character from the admixture of air. If the bronchioles are affected their calibre is occupied by a thickish, muco-purulent secretion. If the alveoli are also involved in this process, their yellowish-white contents may simulate the presence of tubercles, especially when they lie immediately under the pleura. By puncturing them and press- ing out the contents we may guard against this delusion. If a general or circumscribed pneumonia, or atelectasis have occurred, or if the retrograde products of inflammations are present, such as retraction and thickening of the interstitial tissue, and dilata- tions of the bronchi, then the appearances indicate the features peculiar to these processes, the discussion of which belongs in the section which treats of them. The younger the children the more frequently is stripe-pneumonia found. If there has been pleurisy, the pleura in the inflamed region is found thickened and dulled, and overlaid with more or less fibrinous exudation. It is not unusual to see numerous ecchy- moses on the pleura, especially on the posterior surfaces of the lungs. The pericardium is also sometimes the seat of such effu- sions of blood. Emphysema will seldom be found absent in the lungs of a child that has died from whooping-cough and its results. Its seat is generally marginal and peripheral. Less frequently it is found to have extended to the interstitial tissue of the lungs and the cellular tissue of the mediastinum. If the air has thence been diffused into the subcutaneous cellular tissue of the surface of the body, we cannot fail to recognize this in the elastic tumor which is presented, yielding on pressure, and giving rise to a peculiar sound. If pneumothorax has resulted from subpleural emphysema the half of the thorax affected is found to be en- larged, and the intercostal spaces distended. If no adhesions of the surfaces of the pleura already exist, the lungs are found to be pressed inwards, backwards, and upwards by the air that has PATHOLOGICAL ANATOMY. 711 escaped. Pleurisy need not necessarily have followed a pneu- mothorax arising in this way. ( In some cases I have found one or more circumscribed apo- plexies in the lungs which had been evidenced by no symptom whatever during life. The subjects of oedema, chronic pneumonia, acute and chronic miliary tuberculosis, endocarditis, pericarditis, menin- gitis, acute tuberculosis of the pia mater, croupous laryngitis, and oedema of the glottis must be sought for in the sections devoted to them. Letzerich1 claims to have proved the exist- ence of masses of whooping-cough fungi in the dilated alveoli of the lungs. Hyperplasia of the tracheal and bronchial glands, often with cheesy degeneration and breaking down in the centre, is to be demonstrated in almost every corpse after tussis convulsiva. It is not unusual for a like condition of the mesenteric and retro- peritoneal glands to be associated with it. If the children have died before the disease has passed into the third stage, in the great majority of bodies the ulcer on the under surface of the tongue will not be absent. I have once seen diphtheria of the tongue. In the brain, in its membranes, and between these may be found effusions of blood of varying size. (Edema of the brain is almost constant, as is also exudation into the ventricles, and between the membranes of the brain and also those of the spinal cord. If general dropsy has taken place, there are effusions of variable amounts into the pleural cavities, the pericardium, and the peritoneal cavity. If the patients were not extremely emaciated, the liver is more or less hyperaemic. Isolated peripheral foci of liver-cells laden with fat are rarely absent, especially in young children. Less frequently, although this is the rule in rachitis and chronic tuberculosis, this accumulation of fat is general, the liver is con- siderably enlarged, and incisions through the yellowish-gray organ leave the blade of the knife covered with fat. The bile in these cases is generally scanty and clear. I have constantly found the mucous membrane of the oe=5o- 1 Virchow's Archiv, Vol. 49. 712 STEFFEN.—WHOOPING-COUGH. phagus pale, and not swollen. The mucous membrane of the stomach, however, is often the seat of catarrhal inflammation, reddened and swollen. Inflammation of the follicles of the intes- tine, as is very apt to be found in all diseases of childhood, is not unusual in this disease. Sometimes I have seen considerable follicular ulcerations at the ileo-caecal valve. It has as yet been impossible to establish the existence of any pathological process involving the kidneys. Conditions depending on general lesions of nutrition, such as rachitis and scrofula, and on the acute exanthemata, are referred to in the sections treating of thern. Diagnosis. It is not generally easy to confound whooping-cough with any other disease. The first stage may, it is true, be taken for a simple catarrhal bronchitis, especially if no epidemic of whoop- ing-cough is prevailing, and if it is not known that infection has been rendered possible. Sometimes the violence of the fits of coughing attracts attention. In like manner the third stage may simulate a catarrhal bronchitis, which is subsiding, if it is not known that spasmodic attacks have previously occurred, and if the ulcer which may have been present on the under sur- face of the tongue has already healed. The spasmodic stage is sufficiently characterized by the aura which precedes the attack, and which is evidenced by tickling in the throat and a feeling of oppression in the chest; by the con- vulsive expirations, with the whistling inspirations that take place between them ; by the extreme cyanosis, often by hemor- rhages ; by the expectoration, especially toward the close of the attack, of bronchial secretion, and by the vomiting ; by the absence of fever, and by the ulcer of the tongue, which is pres- ent in the majority of cases. In the free intervals, the swelling and pale color of the face betray the attacks which have gone before. The attacks caused by the presence of a foreign body in the larynx or deeper air-passages show the greatest resemblance to those of whooping-cough. The sudden onset of the attacks, without an antecedent catarrhal stage, points to this process. DIAGNOSIS. 713 The laryngoscope gives us information of the retention of the foreign body in the larynx. In such a case, too, the attacks of coughing are of the most violent character. If the body is mov- able in the trachea or large bronchi, this fact can be determined by auscultation. If it has plugged a smaller bronchial twig, this can be proved by the sudden cessation of the respiratory murmur in the affected region of the lungs. I have never observed convulsive attacks of coughing in chil- dren in consequence of elongation of the uvula. As whooping- cough is rare in adults, there will scarcely be an opportunity given of confounding these two processes. Examination of the mouth, moreover, would save us from this error. Barthez and Rilliet assert that tracheo-bronchitis in the even- ing, especially in very young children, and suffocative bronchitis may have a delusive resemblance to wiiooping-cough. It may happen that the crying of small children with cough makes it appear spasmodic. Further than this, in suffocative bronchitis a considerable cyanosis may be present, and more or less marked obscuration of the sensorium with seizures of cough occurring spasmodically. Both processes, however, are accompanied by fever, which generally has evening exacerbations. The long- drawn whistling inspirations between the spasmodic expirations are wanting. There are no free intervals ; on the contrary, a certain degree of insufficiency of breathing is constantly present. The attacks do not end with vomiting. Physical examination makes known what is going on in the air-passages, and if it is associated with tussis convulsiva, the characteristic seizures of the latter are apt to become milder. The same authors assert that whooping-cough may be con- founded with the stage of resolution of some pneumonias, if their progress is marked by abundant moist rales, or with tuber- culosis of the bronchial glands and lungs. It will be difficult for any one to take the stage of resolution of pneumonia for whooping-cough. The cough which occurs with the former is not to be compared with the attacks of the latter. A thorough physical examination of the respiratory organs, which cannot be made too often nor too carefully in whooping-cough, will secure us, moreover, against this error. 714 STEFFEN.—WrHOOPING-COUGH. Tuberculosis of the bronchial glands cannot be diagnosticated during life, and therefore cannot be confounded with whooping- cough. Just as little are we to assume the existence of hyper- plasia and cheesy degeneration of these glands, unless the tra- cheal or cervical glands are similarly affected. Moreover, spas- modic attacks of cough, as in whooping-cough, have never yet been established as depending on disease of the bronchial glands. As regards tuberculosis of the lungs, this, as is well known, cannot be determined by physical examination, for the simple reason that miliary tubercles of the lungs stand in no direct relation to the respiratory passages, and therefore can cause no alteration of the respiratory murmur. Even tubercles situated in the mucous membrane of the trachea, bronchi, or their ramifi- cations are not to be diagnosticated by physical examination. Acute miliary tuberculosis of the lungs, unless the pia mater is involved, and its symptoms are overwhelming, may in the vast majority of cases be determined with certainty by the excessive frequency of breathing, if no other reasons for this are present, and if in general other diseases can be completely excluded. Chronic tuberculosis diffused throughout the body may be recognized, when other pathological processes are excluded, by the constantly increasing emaciation. Chronic tuberculosis of the lungs occasions a change in the physical signs belonging thereto only when chronic pneumonia has been secondarily developed. In that case, however, the pathological conditions found on physical examination belong to this process and not to the tuberculosis. The cough in acute tuberculosis of the lungs may be teasing and painful from the secondary bronchial catarrh, but it has no characters common to it with whooping- cough. Neither can the cough of chronic pneumonia after tuberculosis be in any way confounded with whooping-cough. Besides, the processes mentioned are accompanied by more or less active fever, they have no free intervals, but a greater or less degree of respiratory insufficiency is constantly present. In chronic tuberculosis, the liver is usually so swollen from a gen- eral excess of fat that its increase in size can be distinctly demonstrated. This swelling of the liver will be found in tussis PROGNOSIS. 715 convulsiva only when pronounced rachitis is present at the same time. Spasmodic cough, as it occurs especially in hysterical women, cannot be mistaken for whooping-cough. It likewise runs its course without fever, but shows itself as an almost constant cough, which cannot be repressed. Thus a great number of such attacks of coughing may occur in twenty-four hours, and in fact this is apt to be the case at night to a greater degree than during the day. Spasmodic whistling inspirations between the expira- tions are wholly wanting. There is no vomiting ; expectoration is generally scanty ; the disease is not contagious. The differential diagnosis of the complications of whooping- cough belongs in the sections where the diseases concerned are treated of. Prognosis. The prognosis is determined by the age and sex of the patients, by individual predisposition, by the strength, the mode of life, the intensity of the infection, and the complications. The vast majority of patients recover their health completely after whooping-cough. Still at various times and places this dis- ease has claimed many victims. In the period from 1838 to 1853 (Biermer, p. 578), of the general mortality of the whole popula- tion of London 3.4 per cent, were from whooping-cough, and from 1821 to 1835 inclusive, according to Roe, about 3.3 per cent. By others from 3 to 10 per cent, of the fatal cases in childhood have been attributed to whooping-cough. C. West compiles the following table of thirty-five cases ending fatally. None died under six months. 5 " between 6 and 12 months. 1 < ' 2 years. 2 < ' 3 a 3 ' ' 4 a 4 ' ' 5 a 5 ' ' 6 a 6 ' ' 7 a 7 < ' 8 u 10 ' ' 11 u 716 STEFFEN.—WHOOPING-COUGH. According to Gibb and Friedleben, by far the largest percent- age of mortality falls in the first two years of life, and it dimin- ishes rapidly in the third. K. Majer* reports that 96 or 97 per cent, of all the fatal cases of tussis convulsiva occur under five years. In the first year the percentage reached 58. Macall estimates the mortality in the first year at 13.25 per cent., after the third year at 2.38 per cent. In another table (Fifth Report of the Registrar-General) West gives the ratio per cent, of children dying of whooping-cough to the mortality of the whole population, as follows : Under 1 year........ 5.6 per cent. Between 1 and 3 years 10.6 " " 3 " 5 " 10.2 " " 5 " 10 " 5.0 " " 10 " 15 " 0.8 " According to Loschner, in 700 cases of whooping-cough the mortality was as 1 to from 27 to 30. Biermer has brought together the statistics of mortality as given by various authors. The results vary between 2.7 per cent. (Kiittlinger), and 15 per cent. (Whitehead), thus averaging 7.6 per cent. The younger the children the more dangerous is the disease. The largest number of deaths are caused by suffocation as a result of extreme spasm of the glottis. The next most frequent causes are effusions of blood and acute exudations into the nerve-centres and their membranous envelopes. In many cases, especially among the poorer classes, owing to their unfavorable surroundings, children lose their strength and sink under maras- mus, sometimes with general dropsy. The older the children are, especially if they have passed their fifth year, the better are they able to endure the disturbances of their health caused by whooping-cough. They much more rarely succumb to those processes which carry off younger children. Still they, as well as the latter, may be seized with convulsions 1 On Epidemic Diseases of Children, in Bayer. Journ. fur Kinderkrankheiten, 1871, I., p. 223. PROGNOSIS. 717 in consequence of morbid irritability of the nervous system, and a high degree of passive congestion of the brain. This condition is, with rare exceptions, fatal, particularly if the patients are still in their first year. Profuse and repeated hemorrhages from the nose and mouth may likewise endanger life from progressive marasmus. A fatal case of whooping-cough has but seldom been observed after the age of puberty. The female sex shows a larger number of fatal cases than the male. Among thirty-five deaths West counts twenty-one girls and fourteen boys. Tables on a large scale, which have been compiled with reference to the mortality in whooping-cough, prove a like proportion with few exceptions. Apart from the fact that many more girls than boys are attacked by whooping- cough, no explanation can be found for the excessive mortality of the former. Miserable weak individuals suffering from chronic lesions of nutrition, such as rachitis or scrofula, and also the periods of weaning from the breast would, in general, call for an unfavor- able prognosis, particularly when the children, from bad circum- stances, are obliged to pass their lives in impure air, with defi- cient clothing and unsuitable food. This is the reason why the poorer classes furnish the largest proportion of fatal cases. The intensity of the infection is not alike in all epidemics. In some the mortality is very great, especially from the compli- cations, while in others very few of the patients die. If the disease occurs sporadically, the cases are apt to run a milder course than in epidemics. In like manner we may venture on a better prognosis in warm weather than in winter, or the begin- ning of spring. Biermer quotes from Witsell, of Charleston, the statement that the negro children in the Southern States of the Union present a very considerable mortality. Among other cir- cumstances the conditions of life would here be of essential influence. The first stage of wiiooping-cough furnishes a very small con- tingent of fatal cases. It chiefly concerns only very young and ill-conditioned children, who may succumb to marasmus before the second stage has developed, for the constant cough and the fever that accompanies the catarrhal bronchitis deprive them of 718 STEFFEN.—WHOOPING-COUGH. sleep and appetite. In very rare cases sudden death may take place even in the first stage, especially in connection with rachi- tis or scrofula, from effusions of blood, or transudations into the nerve-centres. The spasmodic stage furnishes the largest number of fatal cases. The reasons for this have been already spoken of. In the third stage a child does not readily fall a victim to this disease, provided it runs a simple course. Should death take place it is because the strength is gradually spent, and it cannot bear up against the progressive emaciation. Taken altogether, in most epidemics the prognosis of uncom- plicated whooping-cough is decidedly favorable. Quite a sure indication for a favorable prognosis is to be found in the circum- stance of the intervals between the attacks being absolute, for the children are then bright, and retain their appetite. So soon as whooping-cough is complicated by other diseases the prognosis becomes more unfavorable because of the greater depression of the strength. When complicated with croupous laryngitis and oedema glot- tidis, no child has yet been known to survive. Capillary bronchitis and pneumonia form a very serious addi- tion. From a full half to two-thirds of those attacked may be lost. In the course of these complications the more the symp- toms of whooping-cough recede, the more severe does the inflam- mation of the respiratory organs become, and the more unfavor- able should be the prognosis. Increasing apathy, and above all the occurrence of somnolence are very bad signs. Atelectasis may be recovered from if the readmission of air into the alveoli is rendered possible, and then its injurious effects disappear. If this does not happen, circumscribed pneumonia is developed, and the prognosis becomes unfavorable. Marginal and peripheral emphysema may disappear, or may continue without special injury. Interstitial, mediastinal, and general emphysema render the prognosis doubtful, while perfo- ration of subpleural air-sacs and pneumothorax may be regarded as always fatal. On the occurrence of oedema of the lungs death must be looked for with certainty. TREATMENT. 719 The prognosis in chronic pneumonia is generally unfavorable. In rare cases this process is recovered from, with contraction of the connective tissue and the development of dilatations of the bronchi; but the individuals remain feeble through life and pre- disposed to diseases of the respiratory organs. We generally see this complication run into pulmonary phthisis. The pleurisy which accompanies these pneumonias has no special importance. If the patients survive, it gets well, with permanent thickening and adhesion of the pleurae. Whooping-cough, when complicated with pericarditis, endo- carditis, and meningitis, runs a fatal course, as also when com- plicated with chronic or acute tuberculosis. Disturbances of digestion, such as catarrh of the stomach and bowels, in themselves involve no danger. In feeble subjects, however, the loss of appetite and the profuse evacuations may become of importance from the loss of strength they cause. We are particularly glad to see vomiting, because it brings the attack to an end. Besides this, it is useful in capillary bronchi- tis, by preventing the accumulation of the bronchial secretion, which might lead to the development of atelectasis or circum- scribed pneumonia. Too frequent vomiting may act injuriously, both by the act and by the rejection of food. Marked swelling of the liver is a sign of rachitis or chronic tuberculosis, and therefore of unfavorable prognosis. Complications with the acute exanthemata influence the prognosis unfavorably. This is especially true in regard to measles, the more so as capillary bronchitis and pneumonia are apt to show a special tendency to develop on these two processes as a foundation. Hemorrhages into the organ of hearing and chronic catarrh of the Eustachian tubes or of the cavity of the tympanum may result in persistent hardness of hearing or deafness. Treatment. There are not many articles in the materia medica which have not been advised and employed against this disease. As we possess no specific which would be capable of putting 720 STEFFEN.—WHOOPING-COUGH. an end to whooping-cough, except in a few instances, we must pay more attention to prophylaxis than in many other circum- stances. If this disease is of spontaneous origin, we are unable to exercise any influence upon it. But, since it is of a contagious nature, we must exert ourselves to prevent any infection. With this object, it is of the first importance to prevent persons who are suffering from whooping-cough from meeting those who are well. It is therefore necessary to isolate such patients in private life as well as in hospitals, and not to allow well people to enter the rooms in which patients have stayed. We must be the more prudent in these respects if we have to deal with persons who would be likely to have the disease in a severe form. Among such may be classed children in their first year and delicate, feeble persons, especially such as have suffered from chronic dis- turbances of nutrition or have been exposed to changes in their nutrition owing to weaning ; also children who are suffering or have recently suffered from the acute exanthemata, whose respiratory organs are diseased or have been impaired by disease ; and, finally, such subjects in particular as have been weakened by any pathological process whatever and have not strength enough to offer resistance to a new disease. If infection is to be feared, children must be carefully watched, so as to avoid any chilling or any cause which would be likely to occasion disorders of digestion. If the family is in a position to remove with its children from the locality in which whooping-cough prevails, this is the surest way of protecting them. Besides, it is certain that epidemic cases are more readily infectious than sporadic ones. No catarrh of the respiratory organs is to be regarded as trivial during the prevalence of whooping-cough. The prophylactic employment of vaccination, of belladonna, and of preparations of chlorine has proved delusive. If infection has taken place and the first stage of whooping- cough has set in, there is no remedy known to us by which we can certainly or even probably arrest the further develop- ment of the process. An attempt may be made to take the children away from the locality of the disease and seek a healthy atmosphere. Also the results of inhalations of nitrate of silver TREATMENT. 721 and of salts of quinine, and of the internal use of the latter call for further experiments. Otherwise we must confine ourselves to keeping the patients quite warm and in a uniform but pure air, since this, as well as the spasmodic stage, are rendered worse by impurity of the atmosphere, especially by carbonic acid, dust, etc. In mild weather patients may with advantage be allowed to be much in the open air, but should return home as the sun goes down. Let the patients be well fed, in anticipation of the disturbances of nutrition in the spasmodic stage, and see partic- ularly that the digestion is kept in good order. When there is active catarrh, expectorants, such as certain kinds of teas, sul- phurated antimony, ammoniacal solutions, ipecac, etc., will not be out of place. If the attacks of coughing are violent and painful, we give belladonna, opium, morphine, or hydrate of chloral, in suitable doses. During the spasmodic stage we must, in the first place, help the children in the attack. If they lie down, set them up and support their heads. Cold compresses upon the forehead and on the chest are said to moderate the attack. I have never seen any advantage from them. At the time when the ideas of the humoral pathologists pre- vailed, emetics and cathartics played the chief part. Fr. Hoff- mann, Hufeland, Cullen, and others were enthusiastic for the former, and allowed them to be employed often in excess—some, every second day. Although this method was abandoned long ago, it may still do good service in cases where the air-passages, particularly the bronchioles and alveoli, are overwhelmed with secretion, in consequence of which the respiratory insufficiency is extreme, and we are apprehensive of a secondary pneumonia. Ipecac, sulphate of copper, or subcutaneous injections of apo- morphine are here the most suitable. Tartar emetic would excite diarrhcea too readily. Cathartics are now thought to be required only in passive congestion of the brain and in delayed digestion. During the attacks nothing can be done, for at this time the children cannot swallow. Niemeyer's proposition of prevailing on children to repress the attack when it is coming on only results in its breaking out the more violently. If the children VOL. VI.-46 722 STEFFEN.—WnOOPING-COUGH. become stupefied during the attack, we shake the body, sprinkle cold water upon the face and chest, rub the body, apply sina- pisms, and place the patient in a warm bath, or even, without this, employ cold affusions to the head and neck. In strong, full- blooded children, if an extreme degree of cyanosis remains, in spite of everything, or if there is a lethargic condition, wiiile the veins of the neck are fully distended, we may determine in very rare cases to apply leeches to the head. General convulsive seizures demand the same treatment. During the attack nothing can be done for hemorrhages from the nose and mouth ; after- wards they require the ordinary remedies. Zaniboni advises especially ergot, others the solution of chloride of iron, etc. As the mucous membrane of the air-passages is the real seat of the disease, we are desirous of acting directly upon it. It is therefore our first duty to remove the patients to the purest possible air. If the place of residence cannot be changed, which would be the most desirable thing, and in regard to which especially a stay at the sea-shore is recommended by the older and also by modern authors, then during warm weather patients must be much in the open air. If this is prevented by the state of the atmosphere, they should not stay in their bedrooms during the day. The bedrooms must be aired in the daytime, and the patients must occupy other rooms, which, if possible, must be alternately aired during the day. Cold and stimulating drinks must be avoided, because they irritate the larynx, and may bring on attacks of coughing. Ebenezer Watson1 endeavored to cure the whooping-cough, during the free intervals, by touching the larynx with a solution of nitrate of silver. But the remedy was without result, because it could act on the supra-glottic region only. In spite of this, Pearce maintains, in the Lancet of April 11, 1857, that he has proved its efficacy in seventy-five cases—thirty-two boys and forty-three girls. At the same time he administered nitric acid internally, according to Gibb's method. In the year 1866, in six children over four years old and in two adults, Rehn employed inhalations of a solution of nitrate 1 Edinburgh Month. Journ. Dec. 1849. TREATMENT. 723 of silver at the height of the second stage. At the best, after the third inhalation there occurred a remission of the symptoms, and after from eight to ten inhalations there remained only a simple bronchial catarrh. In the year 1867 I allowed a girl of two years and three months to inhale a weak solution of nitrate of silver twice daily. After nine days a decided remission occurred, with recovery a week later. Brunniche' advises the employment of compressed air. In the year 1860 Roger advised the inhalation of chloroform. The proceeding seems, however, to have had doubtful results. West advises great prudence in the use of it. Clar recommended inhalations of camphor or oil of turpen- tine. I have several times employed the latter in my private practice, and believe that I have noticed good results from it. Kjellberg of Stockholm has advised inhalations of benzine, and Fieber employed with advantage inhalations of a solution of extract of hyoscyamus. Monti expresses himself decidedly against the inhalations of gazeol, which consists principally of ammonia and benzine. [See volume IV. of this Cyclopaedia, p. 420, foot-note.—Tr.] In the year 1862 Hauke published the results of experiments on the inhalation of various gases which he tried in St. Ann's Hospital at Vienna. Oxygen and illuminating gas never in- duced attacks of cough ; on the contrary, after a short time patients were glad to inhale them. Carbonic acid and ammonia made the attacks worse ; they were frequently brought on by hydrogen and nitrogen. He advises increasing the oxygen of the atmosphere in which patients stay, either chemically or by setting out certain plants. Lochner2 sent forty-three children into the purifying cham- bers of a gas-works so that they could breathe the exhalations of the lime used in purifying the illuminating gas. Twenty-three boys and twenty girls were subjected to this treatment, eleven of them being less than a year old. The results are said to have been for the most part favorable. ' Bibliothek for Laeger, Jan. 1867. 2 Bayrisch. arztl. Intelligenzblatt. I. 1865. 724 STEFFEN. —WHOOPING-COUGH. Commenge1 sent eighty-eight children to the gas-works of St. Maude. Of these fifty-four were cured, twenty-four im- proved, while in ten no result could be determined. Each sitting lasted about two hours, and each successful case required on an average eleven or twelve sittings. Maingault," Blache, Bergeron, Barthez, Roger, and Bouchut have declared against making this use of the gas-works, partly from the want of results, and partly because they regard these inhalations as hazardous. J. Grantham has recommended the vapor of the water of am- monia in boiling water. The spasmodic stage is said to have come to an end after three or four days. In the years 1864 and 1865 I directed the employment of inhalations of simple wrarm water sometimes, or of solutions of chloride of sodium alone, or in combination with wine of opium. I gained yet more from inhalations of a solution of tannin with wine of opium. Still the improvement consisted less in the shortening of the whole disease than in an alleviation of the attacks, and more in respect to their intensity than to their number. The details can be referred to in the Journal fiir Kin- derkrankheiten. Vol. XLVI. 1866. p. 6. In the winter of 18681 directed the inhalation of the infusion of ergot for a boy of a year and a half. On the fourteenth day after beginning to use this remedy, there occurred a decided ameliora- tion of the attacks, and thirteen days later the child was cured. In recent cases of whooping-cough, Lesser3 has directed the inhalation of petroleum with benefit. Letzerich,4 acting upon his theory that whooping-cough is due to the reception and subsequent development of fungus spores, directs the inhalation of muriate of quinine in the form of a pow- der in combination with bicarbonate of soda and gum-arabic. According to his report of three cases treated in this way, the convulsive attacks are said to diminish after from eight to ten days, and even the third stage to come to an end soon. 1 Bullet, de l'academ. XXX. p. 9. Oct. 15, 1864. 2 Gaz. des Hopit. 121. 1864. 3 Allgem. med. Centralzeitung. 49. 1873. 4 Virchow's Archiv. Vol. 57. TREATMENT. 725 In the year 1869 I treated a girl of three years and a half by inhalation of a solution of sulphate of quinine. Unfortunately, the parents took the child out of the hospital before any result could have been looked for. Burchardtl recommended the steam from solutions of carbolic acid of from one and a half to two per c Consult also the case of Rollett, Wien. med. Ztschr. 1862. No. 19; also Hebra, in Virchow's Hdb. d. spec. Path. u. Ther. 1865. 906 WAGNER.—DISEASES OF THE SOFT PALATE. The treatment of all the anginas just described is like that of ordinary catarrhal angina. 4. PHLEGMONOUS ANGINA. Phlegmonous angina occurs in several grades of severity which have no sharply marked lines of demarcation. Further, the slighter grades pass over in every gradation into the higher grades of catarrhal angina, and the higher grades pass imper- ceptibly into gangrene of the soft palate. The slighter and middle grades of phlegmonous angina occur both primarily and secondarily from the same causes as those which produce catarrhal angina, and occur to the same extent. Not unfrequently they affect the same individual several times. They are less frequent in childhood, more frequent at puberty and in manhood, infrequent in old age. The higher and highest grades seldom occur from the same causes: sometimes they oc- cur in scarlatina, and, finally, under a few special conditions, which, when of slight intensity, may also excite slight phlegmon- ous angina. These are, in the first place, high temperatures ; the inhalation of very hot air or of flame by persons whose clothes are burning, or who are in immediate proximity to a conflagra- tion ; the inhalation of hot steam or the swallowing of very hot water, most frequently observed in England in the persons of small children who steal drinks from the long-nozzled tea kettle; the application of the hot iron in surgical operations deep in the mouth, etc. Furthermore, phlegmonous angina occurs in voluntary or accidental poisoning with concentrated acids (most frequently sulphuric acid, less frequently nitric, muriatic, and other acids) or alkalies, most frequently with caustic lye, which is kept for washing and other domestic pur- poses, seldom with phosphorus. » Recently Fraentzel observed (Berl. klin. Wschr. 1874. No. 9) phlegmon of the palate, pharynx, etc., after the internal use of liq.ferri sesquichlor. in typhus. Phlegmonous angina, in its lower grades, is characterized, anatomically, by a moderate, and, in the higher grades, by a PHLEGMONOUS ANGINA. 907 much more intense hyperaemia, connected with more or less fre- quent hemorrhages, but chiefly by a more severe and uniform swelling of the tissues, not confined to the submucosa alone. In most instances the soft palate is affected by it in its entire extent; less frequently the affection is unilateral. The swell- ing is the greatest at those points provided with abundant sub- mucous tissue. The uvula may become as thick as the thumb, and the arches of the palate may become so much thickened that the anterior arches may retain an impression from the last molar tooth. The microscopic appearances are various. The blood-vessels are always contorted, dilated, and swollen with blood. In milder cases we find that, beneath the normally adherent or less firmly adherent epithelium, the mucosa is infiltrated with moderately or excessively numerous pus corpuscles, sometimes only in its papillary portion, sometimes in its entire thickness, especially in the neighborhood of the blood-vessels. They are also found in the submucosa, but for the most part in much smaller quantity. The swelling of this tissue is chiefly due to serous infiltration and to dilatation of the lymphatic vessels, especially at the excretory ducts of the mucous glands. The mucous glands themselves are normal, or else considerable quantities of pus corpuscles lie along their excretory ducts and between the acini, while the outer surface of the acini and their cavities are for the most part normal. Hemorrhages and collateral oedema prevail in these cases of phlegmonous angina resulting from external heat. In cases of poisoning the same conditions sometimes prevail, and sometimes there are more or less characteristic alterations of the epithe- lium, the blood-vessels, the mucous glands, etc.1 Simple ulcers on different points of the soft palate, occurring under various circumstances, for the most part without symptoms during life, exhibit as regards their edges and their floors the usual characters of phlegmonous inflammation. The local manifestations in the milder cases are like those of 1 Concerning these last relations, consult the well-known exposition of Rokitansky ; further, Nager, Arch. d. Heilk. 1872. XIII. p. 213. 908 WAGNER.—DISEASES OF THE SOFT PALATE. a severe catarrhal angina. In severer cases they are much more serious. There is intense spontaneous pain, increasing on pressure and on movement, except when gangrene has already taken place, or unconsciousness exists. Deglutition and speech may be in complete abeyance, especially when there is simul- taneous phlegmonous stomatitis and pharyngitis. The tongue is thickly coated for the most part, and strongly retracted in severe cases, as if shortened and thickened. Sometimes there is copious bloody mucus in the mouth. The lymphatic glands of the neck are little, if at all, swollen. The general disturbances consist in fever of moderate inten- sity, with evening exacerbations, and but slightly accelerated pulse, for the most part. The respiration is little hurried in uncomplicated cases, but is increased in various degrees when there is oedema or inflammation of the larynx, etc. Headache is sometimes present and sometimes absent. Vertigo is rarely present. Vomiting occurs frequently, especially in cases from poisoning. The disease usually commences suddenly, even in cases of so-called spontaneous origin. Frequently there is first pain in the throat and a sense of pressure, which rapidly and continu- ously increase, and, according to the cause, at once, or in the course of one or two days, impede deglutition to a very great degree. Less frequently the disease begins with chills or rigors—the local manifestations first appearing some hours later. The duration is about one week in ordinary cases of medium severity. In the severest cases death usually occurs before the end of this period; or, if recovery takes place, improvement begins at a much later date. The termination, in moderate cases, is in return to the nor- mal condition, sometimes with a transition into chronic an- gina. In severe cases this termination is less frequent. More frequently death occurs from the poisoning, or from the simul- taneous or subsequent affection of the larynx (especially oedema of the glottis), or from suppuration in the subcutaneous and inter-muscular connective tissue of the neck, or of the mediastinum; or from inflammation of the lungs (catarrhal PHLEGMONOUS ANGINA. 909 pneumonia, or pneumonia from a foreign body), or by termina- tion of the inflammation of the palate in gangrene (poisoning, scarlatina). The diagnosis of phlegmonous angina is easy in itself. But the further question in point is, whether a primary phlegmonous angina is present, that is, one occurring spontaneously or through some poison, or whether it is connected with scarlatina, or whether it is secondary. In the latter instance the question arises whether the angina is secondary to suppuration in the surround- ings of the tissues of the palate, or whether it occurs in conse- quence of abscess situated in the palate itself or more especially in the tonsils. The existence of an angina produced by heat or cauterizing agents is established either by the history of the case, or, in the absence of this, by the burning of the external skin, present at the same time, the cauterization of the mucous membrane of the lips and the mouth, the discover of the remnants of the poison, or the sudden appearance of a violent grade of inflammation. Scarlatinal phlegmonous angina is almost always associated with considerable tumefaction of the tonsils, in most cases with phlegmonous pharyngitis, frequently also with infiltration of the parotid gland, the lymphatic glands of the jaw, and the surrounding connective tissue. The absence of any external cause for the sudden and intense inflammation, the severe gen- eral manifestations (high temperature, rapid, and usually small pulse, severe cerebral symptoms), the eruption on the skin (either just commencing or already distinctly developed), are further- more important in the diagnosis of the phlegmonous angina of scarlatina. The discrimination of phlegmonous angina from collateral inflammatory oedema is frequently possible from the aspect of the parts (pale color, extensive cedematous swelling), but chiefly by its limitation. In angina Ludwigii and in anthrax, which appears in the upper part of the neck, only one-half of the palate is affected ; in abscess of the gum of the back teeth only the anterior palatine arch of the affected side is swollen in most cases. In scarlatina it is very unusual to see one side alone affected, or one side more prominently than the other. 910 WAGNER.—DISEASES OF THE SOFT PALATE. In small children phlegmonous angina may proceed like a severe pharyngeal diphtheritis, with laryngeal croup, so that tracheotomy may be necessary. I saw this occur in a child one year old, in whom death took place after thirty-six hours' sickness, in spite of this operation. On dissection, considerable congestion and swelling of the soft palate was found, with an insignificant amount of swelling of the ventricular bands (upper vocal cords) of the larynx. The mucosa and submucosa exhibited the conditions above described. The swollen epithelium was found to consist of numerous large cells, which contained from ten to twenty pus corpuscles, either uniformly distributed or collected in a large vacuole. The treatment of phlegmonous angina is, in mild cases, like that of catarrhal angina. In severe cases it consists in the administration of draughts of cold water, ice-pills, and cold compresses about the throat. If there seems to be danger of an extension to the larynx, doses of calomel at short intervals are advisable. In the severe pains of larger children or adults narcotics are to be administered. The angina accompanying glanders, and that accompanying anthrax, may be regarded as further, infrequent modifications of phlegmonous angina. In the angina of glanders the local manifestations are those of an intense phlegmonous angina, sometimes with the produc- tion of pustules and ulceration, or with transition into mortifica- tion, and with great swelling of the tymphatic glands of the jaw, sometimes with considerable oedema of the face and neck. The local disturbances are marked, the general manifestations severe. In the angina of anthrax similar conditions exist; sometimes with gangrenous emphysema of the skin of the neck. In both classes of cases the etiological conditions, the occupa- tion of the patient and the previous local manifestations, are of considerable importance in diagnosis. The prognosis is almost absolutely unfavorable. (See Gangrene.) Psoriatic angina, psoriasis of the soft palate, I have seen occasionally in general non-syphilitic psoriasis of the cutaneous surface. It consists in several distinctly circumscribed patches on the soft palate, but little elevated, uniformly reddened, of the size of one or two lentils, and usually not very numerous, the epithelium upon which does not exhibit any essential altera- INFLAMMATION OF THE TONSILS. 911 tion to the unaided eye. The patches remain for weeks and months, and disappear with the eruption on the skin, or be- fore it. 5. INFLAMMATION OF THE TONSILS ; AMYGDALITIS ; TONSILLITIS ; ANGINA TONSILLARIS. The different inflammations of the tonsils require special consideration, partly because they are frequently present alone, and partly because their appearance in conjunction with catar- rhal and other inflammations of the palate materially modifies these affections. Inflammations of the tonsils are acute or chronic. They affect either both tonsils or only one of them, in either case affecting the organ in its entire extent or only in part. They may either attack the epithelial structures only, or the glandular structures only, or chiefly the connective-tissue stroma, with the capsule or without it, or several of these tissues together. They seldom occur in normal tonsils, but often in partially or wholly hypertrophied or atrophied tonsils. Etiologically, inflammation of the tonsil is like the ordinary anginas. The same form or different forms of tonsillitis fre- quently affect the same individual a number of times, even as many as from twenty to fifty times during his life—less fre- quently, as a rule, as he grows older—sometimes at longer, and sometimes at shorter intervals, sometimes at intervals of only days or weeks. This frequent recurrence of amygdalitis often has its cause in alterations of the tonsils (retention of secretion in the lacunae, etc.), and often its causes are unknown. The following forms of acute angina tonsillaris are to be distinguished pathologico-anatomically. a. Simple or superficial catarrhal tonsillar angina; super- ficial catarrh of the tonsils ; pure catarrhal inflammation of the mucous membrane of the tonsils. The lacunae and the paren- chyma of the tonsils are entirely unaffected in uncomplicated cases ; but one of these structures will often show a similar slight catarrh, or a retention of the secretion from swelling, etc. of the superficial epithelium, which is slightly infiltrated with serum. 912 WAGNER.—DISEASES OF THE SOFT PALATE. b. Lacunal (according to others follicular) catarrh of the tonsils, usually appears in connection with superficial catarrh; but it is generally of longer duration, and is therefore often thought to be the only change that has occurred. Many cases of so-called angina tonsillaris of mild grade belong here. Indi- vidual lacunae of the tonsil, or all of them, those of normal as well as those of hypertrophied or atrophied tonsils, become filled, under conditions of hyperaemia, with a whitish or whitish-yellow, thin or thick curdy substance, flowing out when thin, but, when thick, removable only with difficulty, or even not at all. This substance consists of epithelium and pus in varying proportions. If these contents do not escape from the lacunae, they frequently undergo desiccation, and sometimes bacteria are developed in various amounts ; fat also is formed, and needles of fatty acid ; sometimes cholesterin, and even masses of chalk in molecular form or in the shape of stones as large as peas. (See below). The yellowish or whitish masses seen on the superficial surface of the tonsils correspond in number, size, form, and distribution with the orifices of the lacunae which themselves exhibit numerous variations : they vary much in number; their form is round or oval, three- or four-cornered, etc. When the surface is not kept very clean, the purulent points are not unfrequently covered with mucoid pus, and thus concealed. Sometimes, upon removal of this substance, shallow, circular erosions of the epithelium become apparent around the yellow points. The conditions are almost always easily recognized on the corpse. In the living subject, especially at the commencement of the disease, it is frequently confounded with herpetic angina, with mild diphtheritis, and with superficial abscess of the tonsil. The parenchyma of the tonsil is affected in different ways. In acute cases it is always swollen in a moderate or severe degree, which is the more impor- tant if the disease occurs in an hypertrophied tonsil. The swelling is produced by hyperaemia and serous infiltration, but in greatest part by the simultaneous proliferation of cells. The tonsils then project beyond the arches of the palate to a variable degree. In chronic cases the tonsil is only moderately enlarged, or not at all enlarged. In addition to the follicular tonsillitis, acute catarrh of the palatine arches is alwTays found, frequently INFLAMMATION OF THE TONSILS. 913 also of the uvula and the soft palate, less frequently of the mucous membrane of the pharynx, and hardly ever of that of the mouth. Tonsillitis of the lacunae heals in many cases by the spon- taneous evacuation of the epithelial and purulent contents of the lacunae, or by their expulsion in efforts of hawking ; or the contents may desiccate, and then become foul, or become cal- careous ; or, as a result of the suppuration of the epithelium, there is a loss of epithelium at points in the lacunae and an adhesion of their opposite surfaces. In this way a diminution of the size of the lacunae results, sometimes amounting almost to obliteration, and then the remaining portion may undergo cystic distention. c. Parenchymatous Amygdalitis seldom occurs by itself, but, as a rule, in connection with superficial inflammation or with inflammation of the lacunae, or it is preparatory to the formation of an abscess. It is either primary or produced by extension of the inflammation from the lacunae or from the adjacent struc- tures. It is frequently found in scarlatinous, variolous, croup- ous, and diphtheritic anginas. Parenchymatous amygdalitis is characterized, in the first place, by congestive hyperaemia of a high grade and serous infil- tration. The tonsils may become swollen to double their normal bulk, and may even exceed this. If the affection involves both tonsils, the entrance into the pharynx is decidedly narrowed, and the uvula is dragged forwards or backwards to allow the two tonsils to approach each other, which they may do till they almost touch. If the affection is unilateral, the uvula is drawn over to the opposite side. The enlarged tonsil projects out of its bed, because it cannot project externally. In this stage there results either return to the normal form or an infiltration of small cells, both in the interior of the follicles and between them, and sometimes also in the inter-lacunal connective tissue and in the capsule of the tonsil. These conditions, likewise, may undergo retrogression, or a new formation of reticulated sub- stance with permanent hypertrophy of the tonsils may result. In other instances abscesses occur in varying number. I have examined parenchymatous tonsillitis several times—twice in its transition VOL. VI.—58 914 WAGNER.—DISEASES OF THE SOFT PALATE. to the formation of abscess, where the hypertroidiied tonsil had been extirpated during the first days of the inflammation. Both times the larger portion of the tonsil exhibited the characters of hypertrophy without inflammation. On isolated places of the capsule, beneath the surface of the tonsil, I found a considerable in- filtration with small cells. This also occurred in several places in the epithelial lining of the lacunae, either there alone or in the adjacent cytogenetic tissue at the same time—in the latter case with escape of the pus into the cavities of the lacunae. d. Amygdalitis with abscess; tonsillar abscess. Tonsillitis proceeding to abscess rarely occurs by itself, but usually at the same time with one of the previously-mentioned inflam- mations. Sometimes it affects both tonsils, sometimes only one, or one in a greater degree than the other. It seldom occurs in young children, but often in larger children and in youthful adults. Amygdalitis with abscess consists in the formation, usually, of several abscesses which do not lie in the lacunae, but in the parenchyma of the tonsil, and seldom remain isolated, but usually become confluent. If the abscesses are near the surface of the tonsil or a lacuna, they perforate the former or penetrate into the latter. The previously existing hyperaemia, and the serous or cellular infiltration of the remaining tonsillar tissue then sub- side, and the tonsil returns to its normal form. If the abscesses are at a distance from the surface, a desiccation of the pus usually occurs, sometimes with final resorption and formation of cica- trices, and, at a still later stage, atrophy of the affected places. The tonsils acquire varied proportions according to the number and size of the abscesses and according to the condition of the remaining tonsillar tissue. The palate exhibits evidences of catarrhal or phlegmonous inflammation, sometimes only in the arches, sometimes in its entire extent. e. Peritonsillar, or retrotonsillar abscess—that is, the forma- tion of abscess in the connective tissue surrounding the tonsils, most frequently between the tonsil and the affected palatine arch, usually the anterior arch. The affection ordinarily involves but one tonsil, sometimes the other also several days afterwards. The abscess may acquire the size of a walnut, so that the arch of the palate at the affected spot is bent forwards as much as half an inch, and the tonsil is drawn towards the middle line, INFLAMMATION OF THE TONSILS. 915 sometimes also drawn downwards. The usual termination of the abscess is perforation, and then rapid return to the normal condition. If the affection occupies the anterior surface of the tonsil, we observe a round projection of dark-red color, which maybe as large as a walnut, and which, at a later period, appears gray at its most prominent part, and then sometimes yellow, the tonsil itself being frequently invisible as a consequence of the great oedema of the palatine arch. The uvula, usually markedly cedematous, is sometimes drawn forwards, or backwards, or to the side. If the abscess occupies the outer or the posterior sur- face of the tonsil, the projection is slight, or there may be none at all; on the other hand, the palatine arches are very cedema- tous, the tonsil sometimes being crowded out of its bed be- tween the arches of the palate. Combinations of the inflammations of the tonsils just described are frequent. An acute or chronic inflammation of one or more lacunae most commonly causes a parenchymatous inflammation or a suppuration of the contiguous tissue, or of the surrounding con- nective tissue, if the lacunae are very deep. The inflammation of the lacunae may irritate the surrounding structures mechanically, by the formation of stones, or, chemically, by the decomposition of their contents. Processes occur here analogous to those in the external skin, where the accumulation of secretion in the hair and the sebaceous follicles (the so-called comedones, miliaria, etc.) excites inflammation of the surrounding tissues, producing the various forms of acne. Clinical Considerations. Superficial tonsillar catarrh gives rise principally to local symptoms. The general symptoms are similar to those of catarrhal angina. Tonsillitis affecting the lacunae, parenchyma- tous tonsillitis, and tonsillitis with abscess, are frequently not to be distinguished from each other at the commencement of the disease, but are usually readily distinguishable after they have existed for a few days. Sometimes they give rise to slight and sometimes to very severe local symptoms, and to mild or severe general symptoms. Both series of disturbances are, as a rule, 916 WAGNER.—DISEASES OF THE SOFT PALATE. slightest in inflammations of the lacunae and in mild inflam- mations of the parenchyma, and most severe in those with abscess. The pathologico-anatomical division of tonsillitis into five different forms, as already described, cannot be clinically carried out in every individual case : 1st, because, not unfrequently, several forms are combined ; 2d, because a minute inspection during life is sometimes utterly impossible (in the case of very young children), and sometimes only possible during the first days of the disease, the difficulty of opening the mouth during the later days, the concealment of the diseased tissues by coat- ings of mucus, etc., interfering with a careful examination ; and, 3d, because the deeper inflammations of the lacunae and the deeper abscesses are not recognizable before section of the tonsil, whether in the living subject or on the corpse. The local symptoms are found either on one side only or on both sides; in the latter case they may be equal or unequal in degree. They consist in a feeling of pressure or pain, usually present even during repose, increasing upon external pressure, movements of swallowing, speaking, hawking, etc., and upon movements of the neck and head. In general, they are greater the more intense the hyperaemia, the greater the swelling and the more rapidly it has formed ; and also, for the most part, the less frequently the affection has previously existed. The pains are variously described according to their nature (pressure, burning, stinging, scraping, etc.), and according to their seat (in the palate, angle of the jaw and vicinity, ear), sometimes without any explanation for these differences from the visible extension of the inflammation. The movements of deglutition are painful and impeded, at first with solid substances and afterwards with fluids also, and, in cases of tonsillitis with abscess, may be almost impossible or quite so for some days. Everything taken flows out of the mouth again, and so also with the copiously secreted mucus and saliva already in the mouth. Speech is painful, incomprehensible, and exhibits the characters of anginose speech in the highest degree ; in unfrequent cases it is lisping. There is difficulty in opening the mouth—so much so, sometimes, that the front teeth cannot be separated from each INFLAMMATION OF THE TONSILS. 917 other. Usually there is also some impediment in the movement of the cervical vertebrae in turning the head. With almost all tonsillar anginas there is hyperaemia or col- lateral oedema of the contiguous portions of the pharynx at the same time. If this extends to the Eustachian tube, there will be noises in the ears and continuous or flying pains in the ears, described by some patients as a very distressing symptom ; if it extends to the entrance of the larynx, there will be dyspnoea, especially on lying down, or paroxysms of suffocation may occur. The encroachment upon the naso-pharyngeal space causes the patient to keep the mouth half open. Hoarseness occurs in some cases. Some patients have a short and dry cough, especially in the recumbent posture, probably from the flowing of mucus into the upper part of the larynx. In ton- sillitis with abscess there sometimes exists, from the second or third day on, ordinary or painful oedema of the submaxillary region, and also, less frequently, of the upper portion of the neck and of the face, on one side. The lymphatic glands of the jaw are, in all forms of tonsillitis, rarely swollen. Extensive swelling of these glands occurs (if the glands had not been previously enlarged) almost only in cases of frequent recurrence and in subacute cases with abscess. The general symptoms are slight, or absent, in superficial tonsillitis, and not unfrequently also in lacunal amygdalitis, at least in adults and in frequently recurring cases ; while they are usually very distinctly pronounced in all other varieties. They consist in fever of different grades, in gastric disturbances, and frequently in head symptoms. Fever is not present in most cases of superficial tonsillitis, in many cases of tonsillitis of the lacunae, anl in some cases of parenchymatous tonsillitis. In the remaining forms, especially that with abscess, there is an increase of temperature of from 1° to 1.5° C. (1.8° to 2.7° Fahr.), or even as much as 2° or 2£° C. (3.6° to 4.5° Fahr.), and moderate acceleration in the frequency of pulse and respiration. The temperature usually reaches its maximum in the first few days, especially on the third day: 39°-40° C. (102°-104° F.) in cases with abscess, below 39° C. (102 F.) in the remaining cases. The fever, as a rule, soon shows moderate 918 W^AGNER.—DISEASES OF THE SOFT PALATE. remissions with evening exacerbations, the latter sometimes occurring at noon or early in the night; both are more marked in case of the formation of an abscess. Sometimes a considerable increase of fever is suddenly manifested after several days of slight febrile phenomena. Defervescence is usually critical, the crises continuing ordinarily from twelve to twenty-four hours. The crisis begins most frequently from the third to the fifth day ; but, in the variety with abscess, mostly from the sixth to the seventh day, or even later. Gastric disturbances occur regularly in the variety with abscess, irregularly in all other forms. The tongue becomes coated from the second day of the disease, especially at its posterior portion. The appetite fails altogether in most cases, or its gratification is rendered difficult by the local conditions of the parts. Thirst is moderate in most instances ; it is greatest, usually, in the earlier days of the disease. Constant nausea is not infrequent, but vomiting is. Intestinal disturbances are rare. In cases of deficient cleanliness a bad breath is frequent. Cerebral symptoms are slight in adults, but in children they are frequently very pronounced. They consist in pains of vary- ing intensity over the head generally, or limited to the forehead, in disturbed sleep with frequent dreams, while during the day- time a more apathetic condition prevails for the most part. Delirium is frequently present, especially at night, in children; less frequently in adults. Convulsions also sometimes occur at the commencement of the affection in children. The general sensation of illness, the feeling of languor, etc., is most marked in the forms with abscess, and, for the most part, it is pretty well marked in the other varieties only when the disease is present for the first time. It has its origin in the local disturbances, in the fever, the inanition and the sleeplessness— the latter being sometimes produced only by the greater secre- tion of saliva and the consequent necessity for swallowing. The commencement of the disease is seldom sudden in the milder forms, but more frequently gradual; in the severer forms it is usually sudden. The latter class of cases generally announce themselves as a general sense of being unwell, early in the morning, before rising, after a somewhat restless night. INFLAMMATION OF THE TONSILS. 919 Upon rising, or during any time of the day, a severe chill may occur, or sensations of chilliness of several hours' duration, followed by heat, thirst, loss of appetite, sometimes vomiting, headache, and occasionally epistaxis. At the same time, often only after some hours, occasionally only after one or two days, the local disturbances in the throat become manifested, slight at first, but usually increasing rapidly in intensity. If the tonsils are examined at this period, they usually distinctly exhibit, sometimes without the previous existence of pain and dysphagia, the evidences of superficial or lacunal tonsillitis—the remaining forms being chiefly characterized by a moderate enlargement of the tonsil. When the affection commences gradually, the first evidences of disease are sometimes the general, sometimes the local disturbances, and sometimes both together. The course of the disease presents no essential stages. The duration is different in the different forms of amygdalitis, varying between two and fourteen and even twenty days and more. The superficial and lacunal forms of tonsillitis continue usually from three to four, at most for eight days. In the latter form some isolated yellowish points frequently remain after the congestion and tumefaction, and with them the local disturb- ances have disappeared. Parenchymatous tonsillitis and ton- sillitis with abscess continue at least a week, frequently a week and a half, and even as long as two or three weeks. The termination is always favorable, except in the smallest children, and in certain very infrequent individual cases in adults. Most frequently complete recovery takes place within one or a few days, or in a few hours, or all at once. The latter occurs only in case of abscess in the tonsil or-in its surroundings, and upon its rupture and discharge ;—patients who, a few hours or a few minutes before, were complaining of severe symptoms, local and general, becoming relieved almost immediately. The point of rupture of the abscess is only occasionally to be seen on inspec- tion ; the patient has expectorated or swallowed odorless or fetid pus, as the case may be, or knows nothing about it. If this takes place during sleep, temporary suffocation may be produced by its penetration into the larynx. In a few days the tonsil dimin- ishes in size, prominence, and vascularity; the collateral hyper- 920 WAGNER.—DISEASES OF THE SOFT PALATE. aemia of the surrounding structures, and the increased temper- ature disappear after a few hours, and the pulse not unfrequent- ly sinks below its normal frequence. At once, or after a quiet night, even without having as yet appeased his hunger, the patient, who previously presented a mournful aspect, feels as if new-born. It is true that often, although complete recovery takes place, a great disposition remains to the renewal of similar disease, which follows, sometimes within a few days, sometimes only after months and years.—Parenchymatous tonsillitis fre- quently passes into hypertrophy, and tonsillitis with abscess into partial atrophy of the tonsil. Cases of fatal termination are exceedingly infrequent. They occur almost only in connection with other severe diseases, and in small children—in both classes of instances as a result of sev- eral days' inanition and the febrile movement. The few remain- ing fatal cases have their cause in extension of the disease to the larynx (oedema of the glottis, etc.), or upon the lateral walls of the pharynx (erosion of large vessels with fatal hemorrhage), or in the descent of pus into the thorax, or in severe cerebral symp- toms the causes of which are not determinable, even by post- mortem examination.1 Chronic amygdalitis, chronic tonsillar angina, presents itself almost exclusively in the form of hypertrophy of the tonsils; less frequently, in that of atrophy of the tonsils, to which one of the previously mentioned five anatomical precedents (superficial catarrh, catarrh of the lacunae, etc.), becomes superadded, some- times in the acute, sometimes in the subacute, sometimes in the chronic form. (See Hypertrophy and Atrophy of the Tonsils.) Chronic ulcers on the surface of the tonsils are seldom of catarrhal or inflammatory nature. They are most frequently syphilitic in origin. The treatment of tonsillitis in superficial catarrh and in catarrh of the lacunae is similar to that of acute catarrhal angina. Most practitioners treat parenchymatous amygdalitis in the same man- ner. Others recommend the application of cold to the sides of the upper part of the neck, the frequent dissolving of bits of ice 'Consult Chassaignac, Gaz. des Hop. 1854. No. 65.—Hauff, Wiirtt. Corr.-Bl. 1863. No. 43. ANGINAS WITH STOMATITIS. 921 in the mouth, and even leeches behind the angles of the jaws. Only in very severe swelling, that undergoes no alteration for days, is it recommended to make several scarifications into the tonsils, and to repeat the operation after a day or two. Abscess in and about the tonsil is treated at first in the same manner—especially so, as its diagnosis is not possible for the first few days. In case of the diagnosis being made, warm mouth- washes and gargles are recommended, and warm compresses externally, if they do not produce headache, or increase head- ache already existing. The much-recommended timely opening of tonsillar abscesses is of little use, because it is very seldom successful, and, even when it succeeds, hardly ever relieves the patient. It is somewhat different in anterior peritonsillar abscess ; but even then the relief to the patient is seldom as great as after spontaneous discharge. Deep incisions are not advisable, owing to the contiguity of the carotid artery. Tonsillar abscess is not to be aborted by any treatment (ice, scarification, etc.) ; venesection is at most to be performed in cases of severe cerebral symptoms in larger children and in adults; tracheotomy may become necessary in case of extension of the inflammation to the upper portion of the larynx. (Case of Puech, Gaz. hebd. 1857. IV. No. 34.) The treatment of chronic tonsillitis is essentially the same. 6. ANGINAS WHICH REGULARLY APPEAR WITH STOMATITIS. A precise discrimination cannot be made between those inflam- mations which affect the soft palate especially, and during which inflammatory conditions of the mucous membrane of the mouth recede, and those in which the reverse conditions exist. Never- theless several of the affections belonging to the latter class deserve a brief consideration in this place also. (For more details consult the articles under Diseases of the Mouth.) a. The so-called toxic anginas, which are produced by tartar- ized antimony, by the internal use of mercury, iodine, etc., are always associated with a tolerably intense stomatitis.l xIMier (Union, 1873. No. 4) describes an intense stomato-pharyngitis, which the patient had intentionally excited by means of cantharides. 922 WAGNER.—DISEASES OF THE SOFT PALATE. b. Aphthous angina always occurs only upon isolated por- tions of the soft palate, while aphthae are found in much greater number in the most different portions of the mucous membrane of the mouth. The greatest differences of opinion still exist concerning the pathological anatomy, etc., of the disease.1 c. Ulcerous angina always occurs with an ulcerous stoma- \ litis (thrush), usually of severe grade. The latter occurs much more frequently without simultaneous ulcerous angina. The characteristic ulcers and general catarrhal inflammation occur upon the mucous membrane of the mouth, especially upon the edges of the gums and the inner surface of the cheeks, fre- quently upon one side only. (See above.) The soft palate, especially its central portion, as well as the uvula in its upper half, occasionally the palatine arches and the tonsils, exhibit in | the earliest days small yellowish spots, or spots as large as an inch square and larger, distinctly elevated (suppuration of epithelium), and usually interrupted by small, regularly dis- tributed red points (excretory orifices of the ducts of the mucous glands). After from three to six days, grayish-red de- pressions are found in place of the yellowish patches (losses of epithelium), and after a few days more the normal conditions are resumed. The local manifestations are those of a severe catar- rhal angina, combined with those of stomatitis. Salivation is very profuse, and the breath usually foul. The lymphatic glands of the jaw are little or not at all swollen. There is little or no fever. The duration of the affection is from two to three weeks. The termination is always favorable. Treatment.—Assiduous cleansing with chlorate of potassa (one part to thirty). Ulcerous stomatitis and ulcerous angina, so-called thrush, have excited the greatest interest for several decennia, partly on account of their relation to scurvy and partly on account of their being often confounded with diphtheritis. I have discussed the subject briefly in this place because I have observed the above- described marked participation of the soft palate in many cases treated in the polyclinic. I have not observed it epidemically or endemically. It also appears to be absent in our barracks. 1 Consult the manuals of Diseases of Children and the work of Billard. Further, Bohn, 1. c. p. 67.—Gerhardt, Lehrbuch der Kinderkrankheiten. 1871. 2 Aufl. p. 368. ANGINAS WITH STOMATITIS. 923 Consult the well-known works of Guersent, Diet, denied. 1827.—Taupin, Journ. des conn. me*d.-chir. April, 1839.—Rilliet-Barthez, 1. c. I. p. 197.—Especially Ber- geron, De la stomatite ulcereuse des soldats et de son identite avec la stomatite des enfans, dite couenneuse, diphtheritique, ulcero-membraneuse. 1859.—Roger, TUnion. 1859. No. 54.— Bohn, 1. c. p. 97.—Hirsch, Hdb. d. hist.-geograph. Path. 1862. II. d. Angina mycotica, thrush of the palate. Thrush (aphthae) of the cavity of the mouth, in severe grades, almost regularly attacks the anterior portion of the soft palate, occasionally pass- ing over the greater part of it, the uvula, the contiguous por- tions of the palatine arches, and the pharynx. Sometimes it forms elevated patches from the size of a millet-seed to that of a lentil, sometimes a tolerably uniform, whitish, milky-looking ad- herent layer, which is interrupted for the most part by red points (mouths of mucous glands). In the masses, which are readily removable, even without hemorrhage when care is exercised, we find the cylindrical and dendritic fibres, individual spores and aggregations of spores of the o'idium albicans, lying in greater part upon the epithelium, but in part distributed through it. The remaining mucous membrane of the palate exhibits the char- acters of a mild catarrhal angina. The local symptoms are also of the same character. For all further particulars, see Thrush of the Mouth. In a case of true dysentery I saw an example of thrush affecting the palate especially, and in its entire extent, the mucous membrane of the mouth being involved in a much slighter degree. The patient recovered from the thrush, de- spite the severity of the intestinal affection, in the course of twelve days. Concerning the histological relations in reference to the epithelium and the mucous membrane, see Wagner, Jahrb. f. Kinderk. N. F. 1868. I. p. 58. Nothing positive is known concerning other mycotic anginas. The micrococci, etc., occurring in healthy persons, on different portions of the mucous membrane of the mouth, the leptothrix, do not appear on the palate of healthy persons ; but they occur frequently in pharyngeal affections of every kind, especially when the superficial surface of the epithelium is not engaged in the process of constant renewal, and when the secretion of the mucous glands is diminished. 924 WAGNER.—DISEASES OF THE SOFT PALATE. Fraenkel (Sitz. d. Berl. med. Ges. vom 29. Jan. 1873) describes a benign mycosa of the pharynx in a student of medicine. White, discrete elevations, as much as 1 mm. in height and as large as the underlying glands, were seen upon the tonsils and upon the glands at the base of the tongue. They did not simulate firm mem- brane, but were more like mould. When removed, they promptly recurred. They consisted of epithelium and many lively, moving micrococci, and of numerous partly moving rods of various lengths. 7. CROUPOUS AND DIPHTHERITIC INFLAMMATIONS OF THE SOFT PALATE. ANGINA CROUPOSA ET DIPHTHERITICA. ANGINA MALIGNA. PHARYNGEAL DIPHTHERITIS. DIPHTHERITIS. The literature of pharyngeal diphtheritis is unusually extensive. I give below only the most important works on the disease in general, and especially its clinical relations. Treatises on the other aspects of the disease will be referred to later. Numerous unimportant works, such as ordinary descriptions of epidemics and endemics, recommendations of remedies, etc., I leave out altogether. In like man- ner, I refer to their appropriate chapters the relations of the accompanying affec- tions of other organs, such as the larynx, kidneys, and nervous system. The older literature, especially the Italian, Spanish, French, and English of the seventeenth and eighteenth centuries, is detailed in the Diet, encycl. des sc. med. by Dechambre, 1866. V. p. 1. 45. The most important are: Ghisi, Istoria delle angine epidemiche dell' anni. 1747 and 1748. Cremona. 1749.—Samuel Bard, Re- searches on the nature, etc., of sore throat. New York. 1771. Among recent works the most important is that of Bretonneau, Des inflamma- tions speciales du tissu muquex, et en pai ticulier de la diphtherite, ou inflammation pelliculaire. 1826.—Further, in Arch gen. de m6d. 1855. E. V. p. 1. VI. p. 257.— Guersant, Art. Angine couenneuse, in Diet, en XXI. Vol. 1821. II. and in Diet, en XXX. Vol. 1833. III.— Becquerel, Gaz. med. 1843.—Empis, Arch. gen. Feb. and March, 1850.—Isambert, Arch. gen. E. 1857. IX. pp. 325 and 432.—Trousseau, Clin. Mgd. 1861. I. Good clinical German works which treat of pharyngeal diphtheritis in general do not exist (except the short descriptions in works on special pathology and on diseases of children). In special respects recommendable are Bartels, Arch. f. klin. Med. 1867. II. \\Z§7.— Wertheimber, Die Schlunddiphtherie. 1870.—Consult also the compilations of Jajfe in Schmidt's Jahrbb. since 1862: CXIII. p. 97; CXIX. p. 236 ; CXLIX. pp. 217 and 321.—Further, Roser, Arch. d. Heilk. 1869. X. pp. 103, 201, 303, and 366. Croupous and diphtheritic angina are characterized by the appearance, always in an acute manner, under mild or severe local and general symptoms, of peculiar whitish elevated patches on the surface of the soft palate—so-called deposits, of varying PHARYNGEAL DIPHTHERITIS. 925 extent, which disappear after a duration of several days, but sometimes reappear upon the same spot. If the tissue beneath the deposit is only hyperaemic and infiltrated with serum, and the lymphatic glands of the jaw are not at all or only a little swollen, the angina is of a croupous nature. If, on the con- trary, the tissue beneath the (slight, or, for the most part, dense) deposit is very hyperaemic, or at the same time hemorrhagic and infiltrated with sero-purulent matter, and if the lymphatic glands of the jaw are considerably swollen, then the angina is diphtheritic. Even in the latter class of cases, the tissues may return to their normal condition after two or more weeks' con- tinuance of the disease. Or they may become gangrenous, involving the palate, especially the tonsils, as well as the lym- phatic glands—so-called gangrenous diphtheritis. The three forms mentioned run into one another in various ways, in their local manifestations as well as in the participation of the system in general. I have wavered for a long time as to whether I should take up .pharyngeal dipththeritis in the description of the diseases of the pharynx, inasmuch as it has already had a detailed consideration in the first volume of this cyclopaedia. I have finally decided to take it up, however, chiefly for the sake of completeness. I could not bring myself to give up writing about that very disease of the pharynx, which has attracted the most general professional interest for the last decade. Furthermore, I take up the subject of diphtheritis because I have followed it with interest since its first appearance in Leipsic, and have closely studied it, at least from one point of view. Finally, I have included it because I differ essentially from Oertel (Vol. I.) in several theoretical points. My description, which is to follow, will be more a picture of diphtheritis at Leipsic, than a general delineation of that disease. On this account I have failed to give an extended review of the literature of the subject as well as an exhaustive consideration of many etiological and general pathological questions. My expe- rience is based upon numerous mild cases, and upon about one hundred fatal cases, for the most part severe, and principally fatal by croup of the air-passages. These were either seen by myself or by Prof. Wunderlich, who has very kindly placed his clinical notes at my disposal. Of these I have made a complete dissection in forty- three instances, and a dissection limited to throat and thorax upon about as many more. All these fatal cases were cases of pure primary pharyngeal diphtheritis and not of scarlatinous diphtheritis. I saw the first fatal case in September, 1856; the second in October, 1861. Cases of the disease and of death from it have become more frequent only since the autumn of 1862, and since this period only has the 926 WAGNER.—DISEASES OF THE SOFT PALATE. disease been known here as pharyngeal diphtheritis. Of the three physicians engaged in the hospital service during the years from 1860 to 1870, each one has to mourn the loss of one, and one of them of two of their own children from diph- theritis. Fatal croup of the air-passages without an affection of the pharynx has occurred much less frequently since that time. I have seen, and in fact dissected, only three cases; while, of the above-mentioned forty-three cases, thirty-nine died essentially from the croup of the air-passages; it was absent in four cases only. The condition of things is similar in Dresden, and also, according to West, in London. The deposit furnishes the most important diagnostic feature in croupous-diphtheritic angina. It shows itself in patches of va- rious sizes, dead-white at the beginning (of a dull silvery lustre, parchment-like, lardaceous), roundish, closely adherent to the subjacent tissue in the early days of the disease, and detachable, for the most part, only at the expense of a hemorrhage. These patches increase in thickness and in area in a few hours, or a few days, and distinctly project beyond the adjacent surface. The latter, as well as the underlying mucous membrane, is dark-red in color. The patches are either sharply circumscribed, or they gradually merge, throughout their circumference or at certain points, into the contiguous tissues ; in the former instance they do not enlarge in area any more, while in the latter instance they continue to increase. The recognition of the deposit is easy in the great majority of cases, if not at the first examination of the patient, at least upon the second, undertaken after some twelve or twenty-four hours. Its recognition is difficult in cases where the deposit lies upon the posterior surface of the palate, or when the surface is covered with mucus, or fluid food (especially milk), and cannot be effectually cleansed, and where cauterization of the surface has already been made with acids, but more especially with nitrate of silver. The deposit is confounded most frequently with the wdiitish plugs which project out of the normal or enlarged lacunae of the tonsils, as well as with the whitish or yellowish, somewhat raised patches which occupy the interior of the lacunas without projecting through their (narrowed or closed) outlets. In both classes of cases the questionable patches occupy only the surface of the tonsils, not the uvula, soft palate, etc.; their size and distance apart correspond with the lacunae; the first-named PHARYNGEAL DIPHTHERITIS. 927 plugs project too much, for the most part, with but a slight ex- tent of surface, and those last mentioned come distinctly nearer the surface after half a day or a day. Less frequently a croupous deposit is confounded with suppuration of the epithelium, as in catarrhal angina, ulcerous angina, etc. (see p. 891), and in variola of the soft palate (see p. 902); or with shallow syphilitic ulcera- tions, beneath which the mucous membrane is anaemic from cellular infiltration ; or with thrush of the soft palate (see p. 923); or with gangrenous processes (which see). Croupous-diphtheritic angina occurs, with many similar char- acteristics, anatomically and clinically, under four different conditions. 1. As a primary disease, the so-called true pharyngeal diph- theritis in healthy persons, less frequently in persons otherwise diseased. 2. As a complication of scarlatina, the so-called scarlatinous pharyngeal diphtheritis. 3. As a secondary disease in the other acute exanthemata (measles and small-pox), in the acute infectious diseases (typhus, cholera, pyaemia, puerperal fever), in various chronic diseases (tuberculosis). 4. As a so-called non-specific angina, with croupous exuda- tion. Pathological Anatomy. Croupous angina is characterized especially by the deposits described. These form smaller or larger patches, or occupy a larger surface. In the latter instance the entire surface of the soft palate, including the uvula and the tonsils, may become covered with the deposit. Not unfrequently it is simultaneously found at the root of the tongue, upon the contiguous portions of the mouth, and upon the pharynx, nose, and larynx. (These do not come under consideration just now.) The deposits, in a recent condition, are white ; they have a dull lustre, and are of varying thickness up to Tfhr of an inch, sharply bordered, firmly adherent to the subjacent tissue at first, and elastic. After a continuance of several days they become gray, even blackish, 928 WAGNER.—DISEASES OF THE SOFT PALATE. turbid, less adherent to the subjacent tissue, and also somewhat less elastic. Microscopically, the fresh deposits consist of a clear, homo- geneous, glistening network of varying thickness, the interspaces of which contain serum, or blood or pus corpuscles. The inter- spaces are for the most part very small; only here and there are they larger, even microscopic. Sometimes the latter is the case in the entire deeper half of the deposit. In the beginning the uppermost, flattened epithelium is still present upon the de- posit ; but after a few days' continuance it will have disappeared. The lowermost epithelial layers are always still present in the beginning, and sometimes remain throughout the entire disease. The croupous network occupies the place of the epithelium, and never extends into the mucosa; but it extends to various depths into the lacunae of the tonsils, though very seldom into the subepithelial portion of the excretory ducts of the mucous glands; even the portions of the excretory ducts lying in the epithelium seldom participate in the formation of the network. The mucous membrane beneath the croup membrane is in uncomplicated cases at first markedly hyperaemic, less so at a later date—sometimes dotted with variously numerous hemor- rhages, for the most part considerably infiltrated with serum, sometimes with sero-pus. Its lymphatic vessels are mostly con- siderably dilated and filled with serum, or—and more frequently —with fibrine and pus corpuscles. Many different views are held concerning the nature of the deposit—the croupous or diphtheritic membrane. Most authori- ties regard it as a fibrinous exudation, which, according to many, is located upon the epithelium, according to others beneath it, and according to others, again, replaces it. Buhl (Verh. d. Bayr. Akad. 1863. II. p. 59. Zeitschr. f. Biol. 1867. III. p. 341) and myself (Arch. d. Heilk. 1866. VII. p. 481) regard it as a product of the epithelium. According to my views, the epithelial cells swell; their protoplasm contains interspaces in numerous different places, which become filled with serum or pus corpuscles, etc., while the remaining portions become par- ticularly clear, glistening, resistant, etc. This metamorphosis does not take place in the uppermost flattened epithelial cells, PHARYNGEAL DIPHTHERITIS. 929 and ordinarily the lowermost ones do not take part in it either. It begins in the upper half of the middle layers of epithelium, and appears to extend thence more rapidly upwards than downwards. In consequence of the metamorphosis mentioned, and of the swelling of the underlying mucous membranes, the affected places project comparatively far, and sometimes, fungus- like, above the surrounding tissue. Not unfrequently globular bodies, which consist of finely punctated masses of fungus, are found in one or more layers, upon the upper surface of the croup membrane, or, when the uppermost flattened layer of epithelium is still pre- served, above this, and later in spots also between the latter and the croupous reticulum. The deep boundary of the croup mem- brane sometimes consists of one or more layers of not materially altered epithelium, and sometimes of the uppermost layer of the mucosa. (The contrary view that the croup membrane reaches into the tissue of the mucosa itself, I have never found con- firmed.) The detachment of the croup membrane occurs after several days' continuance. Either the upper portion alone is thrown off, the membrane splitting in thickness, so to speak, or it is thrown off in its entire thickness. The first method occurs by the appearance in the thickness of the membrane of large spaces filled with serum, hy means of which the network is drawn out into fine threads and finally torn. The latter method occurs by arrest of the metamorphosis at the lowermost layers of epithelium, and in the mildest cases by the continual growth of new epithe- lium. In cases less mild, a penetration of serum takes place between the membrane and the still remaining epithelium or the upper surface of the mucosa. Furthermore1, the croup membrane is loosened from its connection with the tissue beneath it, occasion- ally by the swelling of the latter and the enlargement of its superficial surface, but generally by reduction of its swollen con- dition and diminution of its surface. In both instances rents occur not unfrequently, forming spaces in the croup membrane, which frequently contain at the same time the above-mentioned fungus globules. The mucous glands do not have any essential relation to the VOL. VI.—59 930 WAGNER.—DISEASES OF THE SOFT PALATE. croup membrane. The latter usually comports itself in essen- tially the same manner in places where tliese glands are very nu- merous (the uvula, etc.), and where they are entirely absent (the tonsils). Either the epithelial portion of the excretory duct of the mucous glands (and unfrequently their subepithelial portion also) is at the same time croupous, and thus more difficult to recognize, or it is not altered, or it is even somewhat dilated. Sometimes the croup membrane (less frequently in the palate, often in the larynx and trachea) then exhibits regularly dis- tributed round holes, empty or filled with mucus. These are the excretory orifices lying in the epithelium. Those portions lying in the mucosa are frequently dilated and filled with mucus. The follicles of the glands are normal. Croupous-diphtheritic, or so-called purely diphtheritic an- gina is characterized by the same croup membrane, sometimes re- markably thick, and often extended over a large surface; while the mucosa, in severe cases the submucosa also, the interacinous tissue of the mucous glands, and the intermuscular connective tissue, exhibit a considerable sero-purulent or purely purulent, or thick cellular infiltration, in addition to the hyperaemia and the frequent and extensive hemorrhages ordinarily present. It is worthy of remark that this cellular deposit reaches much further on the surface, in most instances, than the croup membrane, so that sometimes the most posterior portion of the root of the tongue is densely infiltrated with cells, while that region exhibits but little alteration in its epithelium, or even none at all. In the above description I have, like most authors, designated as diphtheritis the deposition of cellular elements in the tissue of the mucous membrane, etc., although the word diphtheria signifies what we now ordinarily mean by croup membrane. I follow in this only the present habitual use of the word diphtheritis, in which its true meaning (skin, membranous) has gradually been lost. Fungus-globules, such as are found in croup, and ordinary micrococci occur much less frequently in the tissue of the mucous membrane and the deeper struc- tures than in croup membrane. I have never been able, in spite of frequent investi- gations in that direction, to confirm the opposite views on this subject announced by some authors, from Tommasi and Hueter to Eberth. (For further particulars, see below.) The lymphatic glands of the jaw, in special cases the lym- PHARYNGEAL DIPnTnERITIS. 931 phatic glands of the entire side of the neck, especially along the external jugular vein, behind and beneath the upper half of the sterno-cleido-mastoid muscle, as well as the glands at the back part of the neck, are always enlarged, sometimes to from five to ten times their normal volume. They are soft, deeply congested, homogeneous upon section, at first grayish or dark-red, later grayish-j'ellow in places. They exhibit the character of a high grade of hyperaemia, hemorrhages in places, and considerable proliferation of cells ; small gangrenous foci are sometimes found in their central portions. The spleen is usually normal; occa- sionally it is acutely swollen.—The solitary follicles of the small and large intestines are often moderately swollen (Rud. Maier, Arch d. Heilk. VI. p. 171).—The liver is for the most part normal to the unaided eye, but sometimes contains the smallest lym- phatic new formations. Consult the remarkable case of numerous lymphomata of various organs, de- scribed by Roth (Virchow's Arch. LIV. p. 254). Gangrenous diphtheritic angina exhibits the same croupous deposit upon the surface, while the underlying portions undergo the already described hemorrhagic, or purulent, or dense cellular infiltration in a high degree, and show gangrenous degeneration in places, most frequently starting from the tonsils. The same alterations occur in isolated lymphatic glands. For the remaining pathologico-anatoniical relations, see further on. Clinical Considerations. A. Primary pharyngeal diphtheritis occurs in several forms, whose extremes can be well defined, while there are many inter- mediate forms. The deposits described are common to all forms, while the affection of the lymphatic glands, the extension to the pharynx, nose, larynx, trachea, and bronchi, the participation of the kidneys, the nervous system, the remaining organs, and the general system, as well as the sequelae, are present in various degrees of intensity, or fail altogether. Our justification in con sidering these various forms as different varieties of one main 932 WAGNER.—DISEASES OF THE SOFT PALATE. affection lies not only in their essentially similar patho- logico-anatomical and histological relations, not only in many clinical peculiarities, but more particularly also in their eti- ology. Every practising physician knows of examples where several individuals of the same family have become affected with croupous angina at the same time, or within a short period, say wdthin a few days of each other—one or more in a severe form, the rest of them in milder forms. The former may die, while the majority of the latter recover promptly and per- manently, with the exception, perhaps, of one, in whom severe sequelae became established. Instances are still more frequent in which the mother or nurse of a diphtheritic patient (both in primary and in scarlatinous diphtheritis) becomes attacked a few days afterwards with a croupous angina, usually of a mild character. Cases of so-called diphtheria, without a diphtheritic mem- brane, are tolerably infrequent. In families where several members are affected with severe or mild croupous angina, one member sometimes shows only an intense hyperaemia of the palate, without any discernible deposit, but, in spite of this, may exhibit later the sequelae of diphtheritis. a. The Milder Forms of Pharyngeal Diphtheritis; Croupous Angina; Pharyngeal Croup. The surface of one tonsil, less frequently of both, from the commencement shows several deposits as large as lentils, which increase in thickness and size from one twelve hours to the next, and usually run together in such a manner that the entire tonsil becomes covered. Only unfrequently does one tonsil alone remain affected ; usually the other becomes covered also on the second day, or, less frequently, on the fourth or fifth day. In the great majority of cases the deposit remains limited to the surface of the tonsil only. In another series of cases it extends from the tonsil upon the contiguous portions of the palatine arches—in some upon the lateral portions of the uvula also. In all the last-named localities the deposit ordinarily remains small in extent, and is usually circumscribed from the commencement. PHARYNGEAL DIPHTHERITIS. 933 Beneath and beside the deposit the mucous membrane is usually strongly injected, dark-red, and moderately swollen. The arches of the palate, as well as the uvula, are sometimes highly cedematous, even without the presence of the deposit. The tonsils swell beneath the deposit usually to double or quadruple their normal volume (parenchymatous tonsillitis : see p. 913), sometimes to such an extent that they flatten the uvula upon both sides. Acute catarrh exists in the posterior portion of the mouth and in the pharynx. The lymphatic glands of the jaw are somewhat swollen in almost every instance, but not to a great degree. The deposit is usually distinctly visible on the first day of the disease. Where this is not the case, it either occupies a position unfavorable to vision (behind the palate, or in the depth of a tonsillar furrow), or it is not yet thick enough to admit of its recognition upon the hyperaemic substratum. It frequently spreads for several days from the localities first affected, or else new deposits take place independently of the old ones. All this occurs more promptly, on the whole, in younger individuals. After from three to four days, frequently not till after six or eight, and sometimes not till after from ten to fifteen days, the deposits become loosened and are swallowed with the drinks or expectorated; those of the posterior surface of the palate may even be sneezed out. The portions of mucous membrane upon which they sat exhibit no macroscopic alteration in the great majority of cases, or they may appear somewhat thinner, and, very seldom, superficially eroded. The local disturbances of the patient are either present from the beginning, or they appear for the first time after the existence of general symptoms of several hours or even of one or two days' duration. They are not distinguishable from those of a moder- ate grade of catarrhal angina, consisting in difficulty of swal- lowing, somewhat nasal speech, slight spontaneous pains, and moderately severe pains on pressure and movement, salivation, sometimes impeded nasal respiration, sometimes severe aural pains. In some cases local disturbances are altogether absent. The general symptoms are very various. They are so slight sometimes that the patient continues his avocation during the 934 WAGNER.—DISEASES OF THE SOFT PALATE. entire duration of the disease, or during the first few days of its course ; children even continue to frequent their schools, and are with difficulty confined to bed. On the other hand, there is sometimes a severe sense of illness from the commencement. Among the special manifestations, the fever is neither typical nor does it bear any proportion to the extent, etc., of the deposit nor to the hyperaemia, etc., of the mucous membrane. On the first day of the disease there is usually a moderately high tem- perature, or it may be quite high from the beginning, from 38.5° to 40° C. (101.3° to 104° F.). This temperature either increases during the following days, say to 41° C. (105.8° F.), or it remains without rising any further, or it decreases by from 1° to 2° C, principally in the mornings. It presents only moderate evening exacerbations. From the fourth to the sixth day, some- times earlier, the temperature usually declines, sometimes from 41° C. to 38° C. (105.8° to 100.4° Fahr.), within one or two days, and the patient is usually free from fever a few days before the disappearance of the deposit. Only very seldom is there a total absence of fever. The pulse exhibits moderate acceleration, proportionate in general to the temperature. In some cases it is unusually high in the first few days, from 120 to 140 in adults, and after a few days it sinks to its normal frequence or even below it. The respiration sometimes corresponds to the frequence of the pulse, and sometimes it is somewhat in excess. The remaining general manifestations depend partly upon the local affection and partly upon the fever. In most instances there is more or less, sometimes excessive, languor and debility, indisposition to work or to play, either from the very commence- ment or after a few days' sickness. Headache, or discomfort in the head, usually of a moderate degree, general or confined to the brow, is frequently complained of by adults. This exists from the beginning or appears only after a few hours or a few days. With it, the countenance is seldom flushed, but rather pallid, the latter sometimes despite strong pulsation of the caro- tids. The alimentary organs are usually markedly affected: the tongue is coated ; the appetite is usually much diminished ; there is slight thirst; seldom vomiting ; constipation is more PHARYNGEAL DIPHTHERITIS. 935 frequent than diarrhoea. The urine is almost always normal. Herpes of the lip or the nose is sometimes found to exist with the commencement of the disease, occasionally in children, more frequently in adults. The onset of the disease exhibits remarkable differences in small children on the one hand, and in larger children and adults on the other. In the latter class of patients, in the majority of cases, there is moderate pain in the throat and difficulty in swal- lowing, bilateral more frequently than unilateral, coming on most frequently early in the morning, after awakening, or upon getting up—less frequently in the evening, and least frequentty during the course of the day or of the night. Sometimes there is only pain at the angle of the lower jaw. Chilly sensations are frequent, downright chills rare. Unfrequently the last two symptoms are present first, the difficulty of swallowing appearing several hours later. Sometimes there is only a general feeling of discomfort, languor, etc., or only headache, or gastric disturb- ances may be most prominent—loss of appetite, nausea, even vomiting. The same initial symptoms sometimes occur in young children, as far as they can be recognized; or there is moderate or severe aural pain, usually unilateral; or the disease may be recognizable only by its local manifestations. The course of the disease usually exhibits no material fluctu- ations. The difficulty of swallowing and the remaining subjective disturbances increase in the following days, so that not unfre- quently professional assistance is not solicited until the third day. With the subsidence of the hyperaemia and swelling of the mucous membrane the local disturbances diminish, although small deposits may still be present. The disease terminates, in ordinary favorable cases, in from five to fourteen days—most frequently at about the end of a week. Convalescence is usually rapid, but it is sometimes slow in children. The complications which appear during the course of the disease are not very frequent, but they are of importance, be- cause the danger in so-called mild diphtheritis is principally due to them. They are: extension of the deposit into the larynx, etc., diseases of the kidneys, very rarely pneumonia, etc. As a 936 WAGNER.—DISEASES OF TnE SOFT PALATE. consecutive disease, paralysis of the palate, etc., occurs, but is likewise infrequent. b. The Severe Forms of Pharyngeal Diphtheritis ; Diphtheritic Angina ; Diphtheritic Pharyngeal Croup. The surface of one tonsil, seldom of both tonsils in the be- ginning, becomes covered, in from twelve to twenty-four hours, with a uniform deposit; or deposits, small and scattered at the beginning, coalesce within a similar period. The deposit, how- ever, does not remain limited to the tonsils, but extends, in one or a few days, upon the arches of the palate, (the anterior arches more frequently), upon the anterior and posterior surfaces of the soft palate, and upon the uvula—sometimes in the form of small isolated patches the size of a lentil and larger, sometimes as a uniform covering over the parts mentioned in their entire extent. The thickness of the deposit, and the marked infiltration of the parts can be determined, in the living subject, by the size of the tonsils and the uvula, and the thickness of the border of the pal- atine arches. The mucous membrane beneath the deposit, and alongside of it, is intensely reddened, and frequently marked with slight hemorrhages. The infiltration of this membrane is of a sero-purulent nature, or composed of small cells compactly arranged ; that of the tonsils consists in a cellular hypertrophy. The swelling of these parts materially narrows the passage between the arches of the palate; this narrowing may be sym- metrical, or one-sided, if there is unequal swelling of the tonsils. Copious amounts of turbid mucus, frequently commingled with blood, are found on all these parts, unless the patient has recently swallowed, or rinsed out his mouth. If the opportunity is presented of examining the palate before the appearance of the deposit, the mucous membrane is seen to be darkly reddened, moderately swollen, and dry. After a number of hours, its surface appears peculiarly gray, in places or in its entire extent. The deposit is still very thin, and the hyperaemic mucous membrane beneath it masks its color. A few hours later it has acquired its whitish aspect, and is distinctly raised above the contiguous surface. PHARYNGEAL DIPHTHERITIS. 937 The deposit sometimes extends from the parts named a certain distance on to the mucous membrane of the back of the mouth, more frequently to the root of the tongue, and, furthermore, upon the lateral, upper and posterior walls of the pharynx, and upon the inferior and posterior portions of the nasal passages. At all these localities it is sometimes in patches, sometimes uniformly distributed. Considerable swelling of the lymphatic glands of the jaw is present in all cases, usually from the second day of the disease. This is at first unilateral, or greater on one side than upon the other, but it seldom continues so during the entire disease. The swelling of the lymphatic glands is a tolerably safe measure of the extent of the process in the tissue of the mucous membrane and of the tonsils, especially when a quiet inspection of the palate is im- possible, as in the case of small children, or when it is not known whether the swelling of the tonsils appeared in connection with the present disease or existed previously. Here, too, as in most diseases of the lymphatic glands, many individual differences are observed. The swelling of the lymphatic glands appears earlier, and is more pronounced on the side on which the affection is most severe than on the other. The lymphatic glands may become as large as cherries or larger; they are distinctly circumscribable at the beginning, but their contour sometimes becomes indistinct at a later period. In the most severe cases the skin on the upper portion of the side of the neck is oedematous, and frequently slightly hyperaemic. Sometimes all the lymphatic glands of the upper and middle portion of the neck are swollen, especially in pharyngeal diphtheria, and when the attack is very severe the skin of the corresponding region is cedematous and hyperaemic. The deposits undergo alterations during the next few days. Besides the increase in surface already mentioned, and which is mostly over after three or four days, there is also an increase in thickness, which is especially distinguishable at the edges of the deposit, and in the increased thickness of the deposit upon the uvula. Furthermore, it becomes dirty white, yellowish or brownish, from imbibition of food and medicaments, soot, etc. Unfrequently it is dirty red from the beginning, from 938 WAGNER.—DISEASES OF THE SOFT PALATE. hemorrhage into the membrane and into the underlying mucous membrane. The elasticity present at first is lost, and the deposit becomes brittle. From this cause, and from the diminu- tion in the swelling of the mucous membrane, its lustre is lost. Isolated portions of the membrane become detached from the fourth to the sixth day—sometimes only superficially, in in- stances in which an increase occurs in the thickness of the de- posit ; sometimes in its entire thickness. The deposit exhibits certain characteristics according to its locality—whether observed in situ on the living subject, or only after its detachment. The uvula is sometimes enveloped by a pseudo-membrane in its entire extent, like a sort of glove- finger or thimble—the latter form being then still easily rec- ognized in the expectoration. The deposit upon the uvula, the soft palate, and the anterior palatine arches is sometimes perforated with regular holes, which are the unaltered but dilated mouths of the excretory ducts of the mucous glands— those on the posterior surface of the palate being sometimes ribbed longitudinally. The deposits on the tonsils, which are usually expectorated in fragments, not in toto, sometimes exhibit prominences of varying thickness on one surface—the under surface; they are the adherent deposits of the lacunae. (Similar appearances exist on the pseudo-membranes from the turbinated bones, the pharynx, larynx, trachea, and bronchi.) The hyperaemia and swelling of the mucous membrane usually become distinctly diminished previous to the removal of the deposit. After this, the affected portions of the mucous mem- brane appear less hyperaemic and swollen, without loss of sub- stance, though occasionally with shallow erosions. The mucous membrane either acquires its normal condition in a few days, or it remains hyperaemic and infiltrated a longer time. In the latter case new deposits often form after a day or two, usually thinner than the previous ones, and more promptly detached. This may recur several times on the same spot, or on different spots, usually small in extent, and in infrequent isolated cases may be repeated for from four to six weeks. Shortly before the detachment of the deposit, and soon after it, the tonsils, in particular, not unfrequently appear to be prac- PHARYNGEAL DIPHTHERITIS. 939 tiealty destroyed, either superficially or more deeply. On the following day it is seen that this was not the case; either the deposit was located upon a spot previously atrophied, or the sur rounding tissues were still considerably swollen. The local disturbances are the same as those of a moderate or severe grade of catarrhal angina. They are slight in some cases ; severer in some; very severe in others. They depend upon the thickness of the deposit and the amount of hyperaemia, as well as upon the swelling and mobility of the palate, and upon the size of the tonsils. They usually increase continuously during the first few days, and are most severe from the third to the fourth day. Difficulty of swallowing is the most prominent symptom. This is especially troublesome, inasmuch as the copiously formed mucus in the mouth and pharynx, and the profusely secreted saliva, necessitate in part frequent hawking, and in part frequent deglutition. Sometimes the chief or the only difficulty experienced is connected with the swelling of the lymphatic glands. Speech exhibits the ordinary changes char- acteristic of anginous affections. The breath of the patient may be maintained odorless by constant cleansing of the mouth and pharynx. In other cases a foul, not unfrequently stinking, gangrenous odor is present, which, however, is promptly subdued by the assiduous employment of disinfecting remedies. The ex- amination of the diseased parts is unsatisfactory, on account of the difficulty in opening the mouth. The general symptoms are present much more regularly than in the lighter forms of diphtheritis. The temperature is very seldom normal; usually it is moderately increased, not unfre- quently much increased, to 40° or 41° C. (from 104° to 105.8° Fahr). This affords, however, no estimate of the severity of the case, except when it continues at 104° and more for several days. In the latter instance, and also when morning remissions fail alto- gether for several days, the prognosis is bad. In some severe cases the coldness of face, hands, etc, is in contrast with the high temperature. The pulse is sometimes moderately, sometimes considerably accelerated; in unfrequent cases it is abnormally slow ; frequently it is small and hard from the beginning. Its acceleration usually continues longer than the elevation of 940 WAGNER.—DISEASES OF TnE SOFT PALATE. temperature. Respiration is always moderately accelerated. Pa- tients frequently assume a half-sitting posture, or they are fre- quently obliged to raise themselves, in order to hawk and to cough with more force. In lying down, especially if there is considerable swelling of the tonsils, or swelling of the nasal mucous membrane, etc., at the same time, the breathing is frequently impeded, noisy, and carried on through the open mouth. The masses of mucus moved in the pharynx by the respiratory current produce a sound audible over the thorax; so that auscultation of the chest does not furnish any safe con- clusion as to the contents of the bronchi. The general strength is but little diminished the first day or two ; but from the third day on it usually becomes greatly diminished. Sitting up is found to be laborious. Sometimes the patients are remarkably pallid from the very first, or after a few days' sickness. The cerebral functions are normal; delirium is infrequent; ill-humor is frequent. Moderate headache as well as vigilance exists in most cases. The alimentary organs almost always evince considerable disturbance of function. The tongue is usually thickly coated. Appetite frequently fails entirely ; thirst is moderate. Some- times there is vomiting ; constipation is more frequent than diarrhoea. The skin is usually very dry. Sometimes there is herpes of the lips. The urine is scanty, dark-colored, and rich in salts ; only the chlorides are diminished in most instances. In about one-third of the cases there is mild albuminuria ; unfre- quently, and mostly in severe cases, it is intense. Thorner (Berl. klin. Wschr. 1869. No. 43) found, in several cases of severe diphtheria, an extraordinary diminution in the chlorides, the same as in pneumonia, without the previous imbibition of large quantities of water. The onset of the disease is very varied, in part arbitrarily so, and in part according to the age of the patient. In some cases it is exactly like that in the milder forms—first, difficulty in swallowing, seldom severe from the beginning, etc. In other cases there are the indications of slight or severe illness for sev- eral hours or for a day, the difficulty of swallowing not setting in until from six to thirty-six hours later. Repealed rigors or PHARYNGEAL DIPHTHERITIS. 941 a chill may also be present. Or there may be vomiting, head- ache, and backache, vertigo, indistinctness of vision, and gen- eral languor. All these may exist to but a moderate degree, and are then usually attributed to some real or fancied error in diet, or they may be more severe, in both cases being associated with moderate or high fever. Or there may be disturbed sleep, sleeplessness and delirium. Or all the symptoms mentioned may occur almost simultaneously, sometimes as Avith one sudden blow. In little children the commencing symptoms are sometimes equally characteristic (convulsions) ; sometimes they are very unpronounced, similar in general to some febrile affection, or a severe coryza ; or the child is peevish, has no desire to play, etc. In the sudden onset of the disease, the similarity with the onset of scarlatina is quite marked, inasmuch as an erythema is some- times present in the beginning upon various portions of the body. Herpes of the lips, existing from the beginning, is tolerably rare ; and still more infrequent are vesicular eruptions on other portions of the body, or hemorrhages of the skin. The local disturbances usually follow the above-described general symptoms on the very first day of the disease. Inspec- tion of the palate usually discloses this on the first day, occa- sionally not until the second. In addition to the high grade of hyperaemia and swelling, the deposit may be seen sometimes covering a considerable extent. The cases are very infrequent in which no evidence of the deposit is to be seen on the first or even on the second day. Either the deposit in those cases is really still wanting, or it is located upon some portion of the structure not visible without artificial aid (the posterior surfaces of the palate, palatine arches, and uvula), or the affection begins in the depths of the tonsillar lacunae. The course of the disease is tolerably uniform when the affec- tion remains limited to the palate. In general the deposit extends more rapidly than in the mild form of the disease. The local symptoms and disturbances and the general affection in- crease day by day until towards the end of the first week, only the fever usually abates earlier. The symptoms mentioned then gradually subside, while the debility and anaemia usually con- tinue somewhat longer. 942 WAGNER.—DISEASES OF THE SOFT PALATE. Recovery takes place in the course of the second or third week. The redness and tumefaction of the palate become less, the deposit loosens and becomes detached, the swelling of the lymphatic glands likewise subsides. The fever decreases, the high temperature declining especially, or greater morning remis- sions set in, while the pulse sometimes still remains frequent. The skin becomes moist, the secretion of urine more copious. The swelling of the face decreases and its pallor is lost, the appe- tite returns, sleep sets in, the general languor gradually disap- pears. In occasional cases only the disease may continue a couple of months and more, in consequence of local disturbances ; new deposits recur, usually diminishing in surface and thickness, ordi- narily with progressively slighter local and general manifestations. The complications arising during the course of the disease occur with varying frequency in different epidemics. They occur much oftener in severe than in mild pharyngeal diphtheritis. They consist sometimes in an extension of the croupous or croupous-diphtheritic processes upon the contiguous parts, some- times in diseases of other organs, especially the kidneys, the nervous system, and the skin. They constitute almost the only danger of non-gangrenous diphtheritis. The extension of the croupous, or the croupous-diphtheritic processes upon the contiguous structures, is very frequent. Extension to the gums, the mucous membrane of the mouth generally, and the lips, and particularly to the root of the tongue {stomatitis, etc., diphtheritica), sometimes produces no local symptoms and sometimes only slight symptoms. Extension into the pharynx, usually in a slight degree upon the lateral and superior walls, and in a severe degree upon the posterior walls, is very frequent; it increases the difficulty of swallowing and the general disturbance, without materially influ- encing the other symptoms. Extension to the Eustachian tubes begets pain in the ears. Extension into the asophagus, and further upon the cardia ami the stomach, occurs very seldom. I have only seen in two instances an extension of the deposit upon the uppermost portion of the oesophagus. West found the oesophagus free, although the stomach was covered with the pseudo-membrane. PHARYNGEAL DIPHTHERITIS. 943 In case of extension into the nose, there occasionally occurs a true croupous deposit, but more frequently a combination of croup and suppuration of the epithelium. The participation of the nose is usually painless. It is characterized less by impeded passage to the air than by a peculiar, usually thinly purulent, greenish discharge, excoriating the contiguous parts of the external nose, and on the first day not perceptibly different from an ordinary coryza. In some cases there is at the same time a moderate oedema of the upper part of the face, especially of the eyelids. Besides the nasal diphtheritis, there usualty exists an intense palatal and pharyngeal diphtheritis. It is quite unusual to find the latter slight while the nasal affection is severe. It may, however, not be at all apparent, and then perhaps exists on the posterior surface of the palate. Occasionally pharyngeal diphtheritis commences upon the posterior surface of the palate and on the nose at the same time, and first extends upon the lateral and anterior surface of the palate on the second or third day, remaining slight at the latter location or extending con- siderably. From the nose the croupous inflammation may extend into one or both lachrymal ducts, and, still further, even upon the conjunctiva, in which case there will be overflow of tears, etc.1 The extension of croupous and diphtheritic angina upon the larynx, trachea, and bronchi forms the chief danger in the first-named affection. The disease of the air-passages is usually purely of a croupous nature, or there may be at the same time extensive infiltration of the mucous membrane of the larynx and upper portion of the trachea—the remaining portions showing evidences of ordinary croup. The extension of croup to the air- passages occurs oftener in children than in adults, and much more frequently in severe than in mild cases of pharyngeal diphtheritis. The relation as to time between the affection of the palate and that of the larynx is a varying one. In one series of cases, probably the majority of th^m, both affections appear at the same time, or the laryngeal affection follows hardly a day later. 1 Consult Hirschberg (Berl. klin. Woch. 1869. No. 3) upon the etiology of conjunc- tival diphtheritis, and its connective relations with the diphtheritic affections of the pharynx and larynx 944 WAGNER.—DISEASES OF THE SOFT PALATE. These are the cases in which distinct evidences of laryngeal croup (long-drawn respiration, frequent dry coughs, toneless, hoarse voice, great disquiet, and pains in the throat) also occur from the second to the fourth day, and symptoms of stenosis become manifest from the fourth to the sixtli day—the latter first ap- pearing, in most instances, on the partial detachment of the croup membrane. In a further series of cases, the symptoms of laryngeal croup first make their appearance at the end of the first week, occasionally still later, even towards the middle of the third week. The period at which croup of the air-passages becomes added to pharyngeal diphtheritis is generally misjudged. This is due to the circumstances that the patients are already suffering from dyspnoea, due to the angina itself, especially in case of simultaneous collateral oedema of the ary-epiglottic ligaments—that movements of the body do not take place to account for the dyspnoea, and that usually, also, the speech is feeble from the pain, etc. Therefore the laryngeal affection is most frequently not recognized, until, upon more or less forcible examination of the child's pharynx, it holds its breath for a long time and then screams. In adults and in older children the croupous affection of the air-passages is attended by much slighter symptoms than in young children. In the case of one of my assistants, Dr. O. B., who died on the fourth day of the disease, pharyngeal diphtheritis of a severe grade existed; the croup of the air-passages extended to the third bron- chial division, and, in places, to the fourth division, without any decisive symptoms of the condition having existed during life. In general, if the deposit on the palate is considerable, the croup of the larynx is considerable also; but in many slight cases of the latter condition a diagnosis cannot be made with certainty. But the reverse condition occurs also; slight affection of the pharynx and intense affection of the larynx being combined. The opinion of some, that primary laryngeal croup never occurs, is erroneous, according to the observations made here. Since the domesti- cation of pharyngeal croup, the number of such cases has at any rate diminished. (Seep. 925.) Pneumonia, as well in the form of lobular (catarrhal) as in that of lobar (croupous) inflammation, occurs usually only in connection with croup of the air-passages. I have seen two fatal cases, verified by the post-mortem examination, as well as several cases which were not fatal, in all of which pneumonia existed in the lower lobes, without simultaneous evidence of croup of the air-passages. The lymphatic glands of the neck, and especially those of PHARYNGEAL DIPHTHERITIS. 945 the jaw, diminish in size with the subsidence of the pharyngeal affection, and usually become normal a few days after; not un- frequently, however, they remain enlarged to a slight extent for several weeks. Suppuration occurs only occasionally in spots, and gangrene still less frequently. Albuminuria seldom occurs in slight cases, but occurs in about half the number of severe cases. It is not, however, pro- portionate to the severity of the disease. It is seldom encoun- tered from the commencement—usually not until after several days, sometimes not until towards the termination of the disease. It is usually slight, continuing but a few days, or irregularly intermittent, so that, in the same case, with a duration of two weeks' sickness, the urine may contain from one-fortieth to one-fourth of its volume of albumen at one time, and may then be free from albumen for a day or for several days. Fre- quently the urine contains a few pale tube casts. In cases where the albuminuria has existed, and also where it has not existed, hyperaemia, enlargement, and diminished consistence of the kidneys will be found on post-mortem examination, and microscopically a strongly albuminous or partially adipose turbidity of the epithelium of the kidneys.1 Consecutive dropsy occurs very unfrequently: Demme (Jahrb. f. Kinderh. N. F. I. 1868. p. 21) saw seven cases, four of them fatal, among forty-two cases of primary non-scarlatinous diphtheria. I have never observed it here. c. The Gangrenous or Septic Form of Croupous-Diphtheritic Angina; Angina Gangrenosa. We find here locally the same deposits as in the form al- ready described, the same or still more decided hyperaemia and infiltration of the mucous membrane, etc., and the same rapid enlargement of the lymphatic glands. The process usually grows more quickly in thickness and surface, on the tonsils, and rapidly extends upon the pharynx and into the nasal passages, sometimes also upon the posterior portions of the mouth and upon the gums. On the first and second day, the local appear- 1 Consult Battels, Mitth. d. Ver. schlesw. -hoist. Aerzte. 1873. VOL. VI.—60 946 WAGNER.—DISEASES OF THE SOFT PALATE. ance does not differ essentially from that of the forms previously described. Several differences, however, make their appearance after the third or the fourth day. The diseased surfaces of the palate and nose bleed either spontaneously or upon very slight provocation—at first moderately, later sometimes profusely; or there appears an apparent, much more unfrequently an actual, superficial, or deep gangrene of the affected places, especially of the tonsils. At the same time the swelling of the lymphatic glands becomes constantly greater, and the overlying skin, as well as the adjoining skin to a considerable distance, is fre- quently hyperaemic, and, to a variable degree, cedematous. I have not myself seen actual destruction of the tissues of the palate in primary diphtheritis, but only in scarlatinous diphtheritis. From the descriptions of most authors it appears that they have not observed actual gangrene upon the corpse, but have taken this for granted from the presence of gray shreds similar to dead tissue, and from the odor. (See also West.) According to Millard (Sur la tracheotomie, 1858) and Peter (1. c.) the blood, in gangrenous diphtheritis, is brown, similar to prune-juice, or liquorice-juice, and leaves marks on the fingers like ink. It is turbid, viscid, and readily absorbed; the coagula are not firm. The secretion flowing from mouth and nose is grayish-yellow, frequently mixed with blood, at first still purulent, later ichor- ous. It first reddens and then corrodes the skin of the lips and nostrils. At the same time there is frequently a gangrenous or cadaverous odor in the entire atmosphere surrounding the patient. This, however, is no indication of gangrenous destruc- tion, for the proper cleanliness of the diseased parts may be impossible for various reasons. The local disturbances are either the same at first as in the previous form, or they are remarkably slight from the beginning. In the former case they diminish with the appearance of the gangrenous manifestations. The general symptoms are particularly characteristic. The temperature is usually high, amounting to 40° and 41° C. (104°- ! 105.8°). At the same time the head, hands, and feet are fre- quently cold. The pulse is always much accelerated, small, empty, not unfrequently irregular. The respiration is usually much hurried, even without the larynx or the lungs being affect- PHARYNGEAL DIPHTHERITIS. 947 ed (in consequence partly of the difficulty in expectorating the mucus that accumulates in the upper part of the larynx, and partly from the swelling of the upper vocal cords—ventricular bands). The patient is remarkably pallid; the face is sunken, especially the eyes—this condition contrasting strongly with the swelling of the neck. The entire carriage of the patient is apathetic and indolent, so that even those usually ill-natured make no special complaint, readily permit an examination, etc. There exists either a great amount of disquiet, or, more fre- quently, slight somnolence. Consciousness is usually uncloud- ed, as appears on one's addressing the patient. Adults have a distinct cognizance of the severity of their disease. The appetite fails completely. The tongue is dirty-red or brown, smooth or thickly coated. Thirst, even, is sometimes slight, while the drinks administered are usually quickly and readily swallowed. Sometimes vomiting occurs regularly after drinking, but it seldom sets in spontaneously. The bowels are constipated, or there may be copious, sometimes involuntary diarrhaa. The urine is usually diminished in quantity, is fre- quently albuminous, and sometimes dark, brownish like beer (containing blood). Hemorrhages take place tolerably often in gangrenous an- gina. They are important sometimes on account of their copi- ousness, sometimes on account of their prognostic signification (thinning of the blood). They sometimes take place from the portions of mucous membrane affected with the croupous-diph- theritic deposit; less frequently from the palate and pharynx ; more frequently from the nose. They sometimes occur in the air-passages and in the lungs, even without croup of these struc- tures ; sometimes they take place from the kidneys and urinary passages (haematuria), sometimes from the genitals, sometimes from the bowels. Finally, numerous smaller or larger hemor- rhages of the skin take place, interstitial or free (from the mouth and from blistered surfaces). If the hemorrhages are copious, the temperature sinks from 1£ to 3^ degrees Fahr., but again reaches its former elevation after from twelve to thirty-six hours. In addition to the extension of the diphtheritis by continuity 948 WAGNER.—DISEASES OF THE SOFT PALATE. of surface, diphtheritic deposits take place at a distance from the palate, especially on the skin, in the gangrenous form, and less frequently in non-gangrenous diphtheritis. Diphtheria of the skin, which was very unfrequently observed in our cases, never appears upon the normal skin, but only upon such portions as have been denuded of epidermis, on accidentally wounded surfaces (intertrigo of small children and fat adults), on sore nipples, on blistered surfaces and incised wounds. The affected portions of the skin present a grayish deposit of vary- ing thickness, finally amounting to several millimetres, and similar to that upon the palate. The parts are painful, a clear or slightly turbid fluid, sometimes offensive in odor, oozes from them. The borders of the skin are bluish-red, and strongly prominent—sometimes erythematous for a considerable distance. Upon these places then appear minute vesicles which run together, burst, and at once become covered with the croupous deposit. In this way the malady may extend over half the length of the body, usually from above downwards. Diph- theritis of the skin is usually secondary to diphtheritis of the pharynx ; the reverse condition of things occurs very rarely. Diphtheritis of the genitals affects the glans and prepuce in boys, the vulva and vagina in girls and women, seldom the uterus ; it also affects the neighborhood of the anus in both sexes.1 The onset of gangrenous angina is in general similar to that of the other forms. Usually, however, the general symptoms are severer from the beginning. The course of the disease exhibits two different varieties. In one series of cases the above-described severe diphtheritis con- tinues for a day or for several days, and the gangrenous form becomes superadded. In another, less frequent series, the angina begins to be gangrenous from the start. After an illness of a few hours the palate exhibits the above-described deposit, which, on the second or third day, extends over the pharynx and nasal passages, followed by equally rapid marked swelling of the 1 See, also, Ebstein, Diphtheritis, eine Gefahr der rituellen Beschneidung (Arch. d. Heilk. 1869. X. p. 393). PHARYNGEAL DIPHTHERITIS. 949 lymphatic glands and the adjacent connective tissue. With this there is high fever and delirium, and in most cases death occurs after three or four days. The almost constant termination of gangrenous angina is in death. It generally occurs rapidly, in the course of a few quarters of an hour, or even minutes. The previous apathy usually con- tinues to the last; less frequently death is preceded by great agitation, anxious tossing about, etc. The pulse and respiration are frequently irregular ; the former is generally rapid and small, rarely abnormally slow. The temperature is occasionally high, as much as 107^° Fahr., but usually it is diminished. Sometimes the skin perspires freely. Not unfrequently death is preceded for a few minutes by convulsions, general or of isolated parts ; or it instantly follows the sudden raising of the patient, whether this act was performed by himself or through the assistance of others. Sometimes the evidences of collapse continue for several days, until finally death takes place despite energetic treatment. Less frequently the patient dies unexpect- edly during convalescence, with or without previous convulsions. The causes of death are sought in various conditions corre- sponding to the principal disturbances present during life (high fever, irrepressible vomiting, hemorrhages, albuminuria, etc.), or to the symptoms manifested shortly before death (failure of pulse, general collapse, etc.); but for the most part they remain ob- scure, even on post-mortem examination. In a series of cases post-mortem examination revealed intense bronchitis, mostly with catarrhal pneumonia; furthermore, dilatation of the heart from fatty metamorphosis, and severe affections of the kidneys. In one case I found numerous capillary hemorrhages in the brain and its membranes, in the heart, and in the serous mem- branes ; in a second, oedema of the glottis; in a third, anaemia of a high grade ; and, finally, in a fourth, gangrene of the lungs. Consult Gerlier, Mort par concretions cardiaques dans la dipth. 1866.— Duchenne, Bull, de th6r. 1870. LXXVIII. p. 173.—Ldwenhardt,Virch. Arch. 1867, XL. p. 296.— Bouchut, Gaz. des Hop. 1872. No. 117.—Mosler, Arch. d. Heilk. 1873. XIV. p. 61.— In regard to the infrequent terminations, consult Heubner, Gesichtserysipel mit Hirn- affection (Jahrb. f. Kinderheilk. 1872. VI. p. 105); Bayer, the same with fatal hemorrhage from the bowel (Arch. d. Heilk. 1870. XI. p. 398.)—Scholz (Wien. med. 950 WAGNER.—DISEASES OF THE SOFT PALATE. Presse. 1865. No. 25) saw diphtheritic angina and retropharyngeal abscess, throm- bosis of the left internal jugular vein and transverse sinus, embolism of the left internal carotid artery.— Guterbock (Virch. Arch. LIII. p. 523) saw emphysema of the skin in a case of diphtheria The diphtheritic paralyses 1 occur more frequently in mild cases of pharyngeal diphtheritis—sometimes even in those receiv- ing no medical treatment, than in the severe forms of the disease. They appear most commonly two weeks, sometimes one week, occasionally three and four weeks, after the healing of the local t processes, and in some cases not until after convalescence. They most frequently affect the soft palate, and consist in paralysis of both motion and of sensation {anasthesia and analgesia); less often they affect the extremities in like manner, with or without the paralysis of the palate; sometimes they are all affected at the same time, or one after the other; prefer- ably the lower extremities only; sometimes the sphincters also. Paralysis of the muscles of the eyes and of the larynx is more rare. Not unfrequently there are analogous conditions of the higher organs: either alone or at the same time with the paraly- sis mentioned, most frequently of the organs of vision (presby- opia, myopia, even total blindness), more rarely of the organs of hearing, smell, and taste. Sometimes there is impotence. After a continuance of the paralysis for weeks or for months, complete recovery usually takes place—death but seldom. The latter fol- lows much more frequently from pneumonia due to the presence of a foreign body, with or without consecutive gangrene—less fre- quently from larger bodies becoming detained in the glottis and in the bronchi, from paralysis of the nerves of respiration, etc. B. Scarlatinous diphtheritis occurs but rarely in some epi- demics of scarlatina, and in others almost as frequently as the catarrhal angina (see p. 901). It sometimes sets in during the prodromal stage, sometimes during the height of the exanthem, less frequently after its disappearance or even not till the end of the second week of the disease. It exhibits the same three forms as are observed in primary pharyngeal diphtheritis. 1 For special information concerning diphtheritic paralysis, see the chapters on Diseases of the Nerves. (Vol. XL) PHARYNGEAL DIPHTHERITIS. 951 Pathologico-anatomically, or histologically, there is no recog- nizable difference between primary and scarlatinous pharyngeal diphtheritis. I have examined the purely croupous forms by detaching the membrane in the living subject, and the diph- theritic and gangrenous forms upon the corpse. As already related (p. 946), all the cases of gangrenous pharyn- geal diphtheritis observed by me were, with one exception, of scarlatinous origin. Gangrene probably begins in the tonsils, in most instances, especially in the depths of the lacunae, and usually extends only over the tonsillar tissue—less frequently over the arches of the palate, etc. I have dissected fifteen cases of scarlatinous angina—three in adults, twelve in children. The ordinary cases of diphtheritis had died during the first week— those of gangrenous diphtheritis, between the second and fifth weeks. Among the latter were two in which gangrenous, par- tially cleansed ulcers on the posterior surface of the soft palate were the only thing found. In one case the purulent infiltration extended through the entire muscular tissue, as well as through all the tissues surrounding the lymphatic glands ; the latter them- selves were little altered. In three cases the lymphatic glands of the neck upon one side were gangrenous, and in one case upon both sides. In five cases there was laryngo-tracheal croup at the same time, bronchial croup being also present in three of them, so that tracheotomy had become necessary twice. In a sixtli case there was such a severe non-croupous laryngo-tracheo-bronchitis, that tracheotomy had likewise been performed. Among the five cases there was croup of the upper portion of the oesophagus in one instance, and of the cardia in another. In most of the later cases of death, there were numerous lobular pneumonias, and also punctated or uniform fatty degeneration of the heart. In almost all the cases the affection of the kidneys was much more intense than I have ever seen it in primary pharyngeal diph- theritis. In one there were numerous abscesses of both kidneys. In the cases that died during the first week, there was lymphoma of the liver—in one case, also in the suspensory ligament of the liver. In one instance there was a cheesy accumulation in the lower lobe of the left lung and in the bronchial glands, with acute miliary tubercles in lungs, liver, and spleen. 952 WAGNER.—DISEASES OF THE SOFT PALATE. Clinically, the presence or prompt appearance of the cutane- ous eruption, the nature of the temperature, the rapidity of the pulse, the frequently peculiar condition of the tongue, are im- portant in reference to the diagnosis of scarlatina. The scarla- tinous eruption of the skin, and that occurring in many cases of diphtheritis, mostly a very fleeting erythema, would not be often mistaken for each other. Concerning the remaining diagnostic indications, see under the head of Scarlatina. From the pharyngeal affection the differential diagnosis can only seldom be made between primary and scarlatinous diphtheritis. It can be most easily made in those instances where the soft palate is very markedly reddened in its entire extent, and is only covered in places with the croupous deposit. It is further worthy of remark that, other things being equal, the diphtheritic anginas appearing in the earlier stages of scarla- tina are less dangerous than the primary forms ; that extension to the air-passages occurs less frequently ; that the anginas appearing in the later stages are more dangerous than those occurring in the earlier stages; that the swelling of the lym- phatic glands furnishes here also a correct measurement of the severity of the pharyngeal affection ; that the affection of the kidneys in scarlatina almost always makes its first appearance in the second week ; and that paralysis and cutaneous diph- theritis are not observed in cases of scarlatinous diphtheritis. The pharyngeal diphtheritis of measles is regarded by many as an affection analogous to that which accompanies scarlatina, while others regard it as a secondary disease (see below). It appears in some localities and in some epidemics. It is not seen at all in Leipzig, or, at least, has not been observed for some decades. On the other hand, secondary ordinary anginas, resembling pharyngeal diphtheritis, occur here in severe measles, as in other severe diseases, always simultaneously with intense bronchitis and multiple lobular pneumonia. Morbillous pharyngeal diphtheritis is manifested anatomi- cally as a croupous or diphtheritic stomatitis, pharyngitis, and, for the most part, laryngitis also. Intense bronchitis, with lobular pneumonia, is almost always present. The diphtheritis sets in either a few days after the breaking out of the cutaneous PHARYNGEAL DIPHTHERITIS. 953 eruption or in the stage of its desquamation; it is least fre- quently developed at the beginning of the disease. Its local and general symptoms are sometimes very definite and sometimes insignificant. The local disturbances are very slight in many cases, and present the usual degree of gravity in others. The course of the affection is sometimes rapid, sometimes slow. The prognosis is mostly that of a fatal termination. Consult West, 1. c. C. Secondary diphtheritis is characterized by its appearance in the course of other acute or chronic affections, those mostly of a severe type and presenting distinct symptoms. It generally manifests but slight local and general symptoms, and is almost always fatal. The acute diseases concerned are typhoid fever, most frequently, pyaemia, puerperal fever, erysipelas, whooping- cough, measles ; the chronic diseases are tuberculosis of the lungs particularly, extensive pleural exudations, chronic diseases of the kidneys (Bright's disease so called, second and third stages), chronic suppurative inflammations of the joints, chronic diseases of the liver, especially in topers. Secondary diphtheritis occurs at all ages. It is mostly of a croupous nature only. The mucous membrane beneath the de- posit is hyperaemic, either not infiltrated at all or slightly infil- trated with pus. The croup membrane seldom occupies the palate or the pharynx to any great extent, but, as a rule, only isolated portions, most frequently the tonsil on one or on both sides, with or without implication of the uvula; or the uvula alone ; seldom the pharynx also, but in the latter case usually the larynx likewise. The deposits are sometimes of the ordinary croupous character, containing usually, particularly in their upper portions, very copious punctiform masses of fungi; some- times there is suppuration of the epithelium at the same time. (Sometimes the microscope reveals the latter condition only, though to the unaided eye a thin croup membrane appears to be present.) The symptoms of secondary diphtheritis vary according to the more or less severe general condition of the patient, and— self-evidently—according to the practicability of a minute local 954 WAGNER.—DISEASES OF THE SOFT PALATE. examination. In the majority of cases the local symptoms are insignificant, or fail entirely. In other cases the ordinary local disturbances of a slighter or higher grade are present. In others, still, the disease of the palate is first made evident by the signs of laryngeal croup. In most instances there is an aggravation of the general condition, especially increase of fever. The discrimination between primary and secondary pharyngeal diphtheritis is easy in most cases, but difficult or impossible in others, even on post-mortem inspec- tion. In the first place, it is worthy of mention that any patient with acute or chronic disease may become attacked with primary diphtheritis at any time, and that then the latter affection may progress in the manner above described. Ouhnont (see below) saw eight patients in one ward attacked by pharyngeal dijihtheritis within a few days; six of them had typhus, and five of these died. Furthermore, cases not rarely appear where individuals, apparently healthy, become attacked with pharyngeal diphtheritis and die, and in whom the previous disease is first recognized only upon post-mortem examination. Among the forty-three post- mortems after primary pharyngeal diphtheritis previously referred to, I saw ten such examples; in four instances I found tuberculosis of the lungs and bronchial glands, in one instance an old pulmonary abscess (apparently remaining after small- pox), in two instances severe pulmonary atelectasis, in two instances extensive follicular ulceration of the large intestine, and in one instance a chronic catarrhal ulcer of the caecum, with a lardaceous spleen. The conditions were somewhat similar in the remaining cases, which were not thoroughly examined. Oulmont, Bull, de la Soc. de Med. des Hop. Sept. 1865.— Peter, Gaz. hebd. 1866. Nos. 26, 27, 30.—#. Wagner, Arch. d. Heilk. 1866. VII. p. 516.— Roser, Ibid. 1869. X. p. 374, describes a real septic or cachectic pharyngeal dipththeritis. — Bahrdt, lb. f. Kinderh. 1870. IV. p. 96: secondary pharyngeal diphtheritis and laryngeal croup after diphtheria of a wound in the skin.—Billroth, Wien. med. Woch. 1870. Nos. 7, 8, 20. D. Non-specific pharyngeal diphtheritis (angine couenneuse simple, of Bretonneau ; Angina with plastic exudation, of Trous- seau ; Angina crouposa communis, of Isambert.) The deposits are the most striking and, in many cases, the most important indication of pharyngeal diphtheritis, to be seen either in the living patient or in the dead subject. They are the most important feature in so-called mild diphtheritis, while infiltration of the tissue of the mucous membrane is the most important in severe and in gangrenous diphtheritis. Croupous deposits, however, have been observed in various PHARYNGEAL DIPHTHERITIS. 955 localities—at times also situated on the palate—which have noth- ing in common with true pharyngeal diphtheritis. These de- posits are exactly like those of diphtheritis, macroscopically and microscopically. They occur but seldom, on the whole, and are in the form of small patches, from the size of millet-seeds to that of lentils, in the catarrhal anginas, especially in lacunal amygdalitis, in which affection they form rings around the orifices of the lacunae. They also appear in the form of large patches upon abscesses in the palatine arches; they occur in the same manner in some cases of phlegmonous angina, ac- cording to some authors in the toxic forms particularly (after mercury—nitrate of silver (?)—ammonia (?); they are also some- times seen in syphilis, in the form of larger or smaller whitish deposits ; they are rarely seen in extensive burns of the cutane- ous surface, in scurvy, hospital gangrene, etc., and after sausage- poisoning (?). In most of these cases the diagnosis between specific and non-specific diphtheritic deposits cannot be made from mere inspection of the palate. In non-specific cases the affection is oftener unilateral, and the hyperaemia and swelling are fre- quently slight. Sometimes specific causes (poison) or simul- taneous cutaneous affections, etc. (syphilis) are recognizable. The deposits sometimes disappear with remarkable rapidity; sometimes they remain an unusually long time. They some- times recur several times in the same patient within a short time, other members of the family remaining free from them, etc.1 Etiology. The causes of primary pharyngeal diphtheritis—those of the other forms we leave out of consideration—have at all times been the subjects of most assiduous investigation, and especially so during the last ten years, when it has been thought possible to produce the disease artificially, and its ultimate origin has been thought to be discovered in the presence of a low fungus. 1 Gubler, Arch. gen. Mai. 1857.— Bartels, 1. c. 956 WAGNER.—DISEASES OF THE SOFT PALATE. For reasons already mentioned (see p. 925), the author avoids, in this place also, a detailed reproduction of innumerable -isolated observations, but brings forward only what he has himself observed in Leipzic, and briefly defines his position with regard to the prevalent fungus theory. Primary pharyngeal diphtheritis has occurred here in patients of all ages, most frequently in those from two to six years of age, less frequently in those under two, very seldom in nurs- lings, even when all their brothers and sisters were affected, never in the new-born. Up to the tenth year of age it is still tol- erably frequent; from this age on it is less so, up to twenty- five and thirty years. Beyond this age it occurs very seldom, or at least almost only in the mildest forms, and it has been observed but a few times in old persons. No difference with regard to sex was observable. On the whole, the diphtheria occurred oftener ' in strong, even fat and well-nourished children, than in debili- tated children. Marshall saw diphtheritis in a new-born child (Schmidt's Jb. CIL. p. 324). ,' So far as the season of the year is concerned, it occur? n somewhat more frequently in the autumn, but isolated ca I were not wanting at any season. During the epidemic of chol use to house, from one member of a family to another, and ?m bed to bed in hospitals. Cases of this character have evi- ntly become much less frequent during the last decennium ; in npzic they have appeared with this intensity in isolated istances only. The following grounds, also, are ordinarily eferred to in proof of its contagiousness, although they are for the most part otherwise explicable: namely, the epidemic and endemic appearance of the disease at times ; the remarkable sus- ceptibility of children ; the fact that several members of a family are often attacked; the fact that nurses and physicians in attend- ance are more often attacked than other people; and perhaps, also, the more frequent occurrence of the disease in the families of such professional attendants. With regard to the simul- taneous miasmatic nature of diphtheritis, the principal evidence is, its attaching itself to certain localities, as has been observed from the time of Bretonneau to the present, and by others also, especially Bartels. Only a few such instances have occurred 1 Read the celebrated descriptions of Bretonneau, Trousseau ; and, further, of Boudet, Arch. gen. Feb. 1842.—Becquerel, Gaz. Med. 1843. p. 687. 958 WAGNER.—DISEASES OF THE SOFT PALATE. here in Leipzic. The best evidence on this subject is an obser- vation, substantiated from several sources, to the effect that when healthy children were brought back to the bed-chambers previously occupied by their brothers or sisters when sick with diphtheritis, especially when the cases had been fatal, or even when they were only brought back into the affected house, they sometimes became attacked by the same disease, either at once during the first few days, or not until after thirty or forty days. There appears, therefore, to be a tenacity to the contagion similar to that of exanthematous typhus, etc. The specific poison of diphtheritis is still entirely unknown. It was first hoped that it would be discovered by attempts at the artificial production of diphtheritis. The possibility of the so- called production of diphtheritis by tincture of cantharides and olive-oil (Bretonneau), by acids, alcohol, nitrate of silver, am- monia, chlorine, corrosive sublimate, etc. (Albers, Duval, Valen- tin, Delafond, and others), no longer requires to be refuted. The impossibility of producing it by ammonia, recently again main- tained by Reitz,1 and by Oertel (1. c), has been demonstrated by Mayer.3 Whether the inoculation of croupous and diphtheri- tic membranes in the artificially opened trachea of rabbits, etc.,3 has produced true croup or true diphtheritis, I am unable to say from my own observations. It is well known that Trous- seau, as long ago as in 1828, and at a later date Peter4 inocu- lated themselves wdth diphtheritis several times on the arm, tonsil, and palate, by means of the lancet, but without result. The parasitic nature of diphtheritis rests upon still weaker evidence. According to the variously conflicting experiments of Tommasi-Hueter (Buhl), Oertel, Trendelenburg, Nasiloff, Klebs, and Eberth, and according to Letzerich and others, bacteria are the essential cause of diphtheria. The botanic characteristics of this fungus are still entirely unknown; the fungus is fre- quently but not regularly found in cases of diphtheritis in the human subject, as it readily adheres to the surface of the de- 1 Sitzgs-Ber. d. Wien. Acad. 1867. LV. 2. Abth. 2 Arch. d. Heilk. 1873. XIV. p. 512. 3 Trendelenburg, Arch. f. klin. Chir. 1869. X. p. 720.—Oertel, 1. c. 4 Etude sur la diphtherie et la croupe. 1859. PHARYNGEAL DIPHTHERITIS. 959 posit, and cannot easily be removed by movements, etc.; the gross anatomical and histological characteristics of human and artificially excited diphtheritis vary in manifold and in part in the most essential points ;—on all these data consult the author s Manual of General Pathology. The incubation period of diphtheritis, according to a num- ber of tolerably well-attested observations, occupies from two to four days (Newman, Coulon, Bartels, Mueller, Wertheimer, Thomas, the author); and this is the same after inhalation of the infectious material as after its introduction through the lips, the nose, mouth, eyes, or skin. Cases have not been observed here like those repeatedly observed in France, where diphtheritic masses brought in contact with the surfaces of wounds produced diphtheritis, which either remained local, or excited pharyngeal diphtheritis. On the other hand, diph- theritis of the skin of the external nose, of the mouth, of the external genital organs in both sexes, of excoriations on other parts of the skin (blistered surfaces, leech-bites) in diphtheritic patients, have also been repeatedly observed here. Diphtheritis has been observed likewise at the corners of the mouths of nurslings where mothers were affected with pharyngeal diph- theritis. The use of the clothing and bedding of diphtheritic patients has also been observed here to produce diphtheritis in the foreskin, the vulva, the arms, and the navel of new-born babes, alone, or associated with the affection in the pharynx. I lost my own son at the age of five weeks in this way, from gangrene of the navel with diphtheritic deposit. The croup-like or diphtheritis-like affection of the wound made in the opera- tion of tracheotomy in diphtheritic patients is very seldom true diphtheritis, according to my observations. The relations of diphtheritis to other diseases will be spoken of here only in so far as it has any practical signification. With reference to the fact that croup and diphtheritis belong together, no doubt can prevail, according to the exposition already given. The relations of pharyngeal diphtheritis and scarlatina are in many ways of great interest in practice; both frequently appear in juxtaposition, etc. In spite of this, no correlation between the two appears to exist; for the grounds 960 WAGNER—DISEASES OF THE SOFT PALATE. of this assertion see p. 925. That scarlatina, with ordinarily mild or with severe pharyngeal diphtheritis, may produce in others pharyngeal diphtheritis without cutaneous eruption—in the attendants, for example—has been repeatedly observed here also.1 It is also of practical importance that having been through the one does not protect against the other.2 Finally, cases have been observed in which patients with gangrenous erysipelas, with gangrenous wounds of the skin, with puerperal gangrene, excited diphtheritis of the pharynx, etc., in other patients in the same wards, or in the attendants. This did not occur here. Pharyngeal diphtheritis, and the diphtheritis of wounds in hospital gangrene, etc., are not identical: Roser in opposition to Robert, Virchow, and others. Lasegue (Traite des angines, 1867) describes a diphtheroid angina. Treatment. Few acute diseases have been submitted to as numerous therapeutic propositions and measures as pharyngeal diphthe- ritis. There is hardly another affection concerning which the views of authors differ so widely. This has its cause in the actual or supposed accessibility of the diseased structures, and in the various views entertained as to the nature of the disease (whether it is a local or general disease from the beginning, a fungus disease, etc.), and in the so-called therapeutic results. Almost every physician of my acquaintance has his own method, his favorite remedy. One method is barbarous to the patient, another is milder, a third is expectant. The views of most observers coincide in this, that the majority of so-called mild cases recover spontaneously; that gangrenous diphtheritis is intractable to every form of treatment; that with us the chief danger of severe angina is its extension into the larynx, and that this extension cannot be prevented by any remedial agency. Where the condition of things permits it, the patient is to be at once rigidly isolated, and, where possible, in such a manner 1 See also J. Braxton Hicks, Guy's Hosp. Rep. 1871. XVI. p. 165. 8 See also Mettenheimer, Memorab. 1869. XIV. No. 8. PHARYNGEAL DIPHTHERITIS. 961 that the plrysician and attendants do not come in any contact with the remaining members of the family, the pl^sician visit- ing and examining the healthy members of the family before entering the chamber of the sick. Although isolation, at the time it is usually instituted, is frequently and perhaps con- stantly useless, it is nevertheless advisable, both out of regard to the sick and the well, and is in accordance with the rules of medical policy. The temperature in the bed-chamber should be regulated in accordance with the degree of fever, and the room should at all events be well ventilated. Local treatment is practised in different ways by different physicians; cauterization in every possible degree, the use of so-called solvent substances, the use of disinfectant remedies, and simple cleansing of the palate and pharynx, being the four methods employed. Cauterization is practised with nitrate of silver in substance or in solutions of various strengths, with concentrated or diluted acids, especially with fuming muriatic acid, also with chromic acid, with caustic potash, pure or variously diluted with water or glycerine, with iodine (Lecointe), with an iron warmed in boiling water (Danvin). This must be done daily, at least once, and where possible twice a day. Cauterization, with solid or liquid substances, frequently acts mechanically more than chem- ically. In children, it not unfrequently results in injury to healthy parts, hyperaemia of these parts, and also collateral oedema of the contiguous parts. The caustic reaches only a portion of the diseased surface. Children are much excited by it physically and psychically ; the pains in the palate are some- times first excited by it or still more increased, and the adminis- tration of nourishment is then accompanied with more resistance. In spite of these drawbacks, cauterization is still much in vogue. Of late years, however, the physicians most experienced in the treatment of the diseases of children, Bartels and others, have expressed themselves in opposition to it. Substances which dissolve the deposit and so remove it, are prescribed by many in the form of gargles, and especially of inhalations. Gargles usually cannot be employed on ac- count of want of skill in using them, pain, etc. Those who VOL. VL—61 962 WAGNER.—DISEASES OF THE SOFT PALATE. put faith in inhalations recommend that they be used tolerably often, every hour or two, a few minutes at each time. Some practitioners waken patients from sleep to administer them. The substances employed have been chosen less from the results of practical observation than from experiment upon membranes removed from the living subject or from the corpse. Lime water, diluted in from two to four parts of water, and lactic acid in from fifteen to thirty, are especially employed. When these remedies are diluted and used frequently, they have at least the merit of cleansing the mouth, palate, and pharynx, and of provoking movements of swallowing. When their employment is painful, or when the patient is very weak, they are injurious. Kuchenmeister (Oestr. Z. f. pr. Heilk. 1863, No. 13 u. 15, 1867. No. 38; Berl. kl Wschr. 1869, No. 49 u. 50) first recommended lime water, since so much employed; and A. Weber (Med. Ctrbl. 1869, No. 22) first recommended lactic acid. Consult also Bricheteau and Adrian (Bull, de ther. 1868. LXXIV. p. 72). Forster (Arch. d. Heilk. VI. p. 521) recommends the carbonate of lithia ; Fraenkel recommends a solu- tion of pepsin. Substances are in use, equally often, to wdiich a specific action upon the diphtheritic mucous membrane is attributed, either disinfectant or parasiticidal. Neither object has ever been realized; the disinfectant action is, in most instances, chiefly a deodorizing one, though a cleansing one also ; the parasi- ticidal action is based upon the undemonstrated parasitic nature of the disease. As a systematic employment of these remedies is impossible, we will mention those best knowm, in the order they happen to occur to us. They are employed in the dry or in the fluid form, by insufflation or by inhalation—in the latter instance several times a day. Those most frequently employed, and by some authors praised as unfailing remedies, are alum, tannin, and sublimed sulphur by insufflation, or chlo- rate of potash (from five to ten grains to the ounce), and carbolic acid (one part to three hundred) by inhalation, or they are painted upon the parts, or used as gargles, etc. Alum as well as tannin is at present less employed. Sublimed sulphur, much recommended by Lagauterie, Barbosa, Jodin, Roger, and others, is regarded by certain authors as a sure remedy. PHARYNGEAL DIPHTHERITIS. 963 Chlorate of potash, prominently introduced by Isambert (Etude chim., phys., et clin. sur l'emploi therap. de chlor. de potasse special, dans les affect. diphth£r. 1856), is more frequently employed than any other remedy. Of late years it has been somewhat superseded by carbolic acid, first recommended by Calvert (Lancet, Sept. I860.), and then by Turner and many enthusiastic German physicians. Sulphurous acid, also, is recommended by Dewar (Med. Times and Gaz. May, 1867), and various sulpho-carbolates by Sanson (Med.-Chir. Trans. 1869. LII. p. 139). In this category also belong the employment of iodine (Warring-Curran; iodine and iodide of potassium aa. gr. iv., alcohol f. 3 iv., water, f. § iv., by inhalation) ; of bromine (Goldsmith-Fuckel; bromine gr. vj., bromide of potassium, gr. xxiv., water f. 3 j., applied by the brush) ; of permanganate of potassa (Lessing and others) ; of cinnabar (Abeille); of peroxide of hydrogen (Stohr) ; of ether (Black) ; of glycerine (Stehberger); of highly rectified spirits of wine (Lovenson), etc., etc. Schwanda recommends the galvanic current to kill the fungus ! The so-called mechanical treatment of diphtheritis—that is to say, the removal of the deposit by means of the forceps, proposed by some authors—is not practicable in an efficient manner. The general treatment is of importance in addition to assidu- ous cleansing of the palate, etc., by frequent drinks, rinsing of the mouth, and inhalations of water or chlorate of potassa in weak solution. The patient should be kept in bed, even in the mildest form of diphtheritis ; and only adults should be allowed to sit up, still remaining confined to the room. The diet should not be low, even if there be high fever ; and, as is self-evident, fluid substances only should be allowed. According to the cravings of the patient, we give milk, warm beer, both of them with eggs, meat, broths, and nourishing soups from the begin- ning ; or, if anaemia be present, good beer, wine, and brandy. If an adynamic condition exist, the latter drinks are to be given often, and in considerable strength. In addition to this we administer iron and quinine, the former most frequently in the form of the ethereal tincture of acetate of iron (from five to fifteen drops every three hours), and in the form of the solution of the chloride of iron (from one to five drops in sweetened water, every two, three, or four hours). The following articles have been much recommended for internal administration, with the idea of their specific action: chlorate of potassa and bicarbonate of soda, alone or with nitrate of soda. Their merit is very doubtful. The same may be said 964 WAGNER.—DISEASES OF THE SOFT PALATE. of the internal administration of balsam of copaiba with cubeb (Trideau), as well as that of cubeb alone (Vaslin). The cold water treatment is justifiable only in case of the con- tinuance of high fever for several days and the maintenance of considerable strength. In severe cases of general debility the transfusion of blood may be tried (Demme). Swelling of the lymphatic glands is treated in the ordinary manner. The extension of the pharyngeal disease into the larynx cannot be surety prevented by any remedy. It is recommended to keep a sufficiently large ice-bag continuously upon the upper portion of the throat, from the commencement of pharyngeal diphtheritis. It is usually well borne, and may perhaps prevent the development of laryngeal croup. Antiphlogistics in any form, derivation by sinapisms, blis- ters, etc., are no longer in use—indeed, they are deemed injurious by almost all practitioners. III. Gangrene of the Soft Palate. Gangrenous Angina. Angina Gangrenosa. Gangrenous angina is either primary or secondary. Secondary gangrenous angina occurs very seldom in ordinary anginas ; somewhat more frequently in many forms of phlegmon- ous, scarlatinous, and diphtheritic anginas ; unfrequently in the inflammations of the palate, complicating measles and typhus. Primary gangrenous angina is still more rare. It corresponds probably to noma of the external skin, of the mucous membrane of the mouth, etc. It can usually be diagnosed with certainty only when the patient has been closely observed from the begin- ning, and when the secondary gangrenous anginas above- mentioned are thrown out of the question, on etiological and clinical grounds. The causes of gangrenous angina are entirely unknown. It occurs more frequently in young persons, poor children especially, than in adults ; weak and cachectic subjects, especially those who have recently recovered from severe diseases (typhus, dysentery, etc.), are those most commonly attacked. The local manifestations are alike in both forms of the dis- GANGRENOUS ANGINA. 965 ease at their height. In secondary gangrenous angina there is usually at first an intense phlegmonous inflammation of the entire soft palate, upon both sides alike, or upon one half espe- cially. Usually as early as the second or third day there are grayish or black circumscribed patches, wirich become trans- formed, after a few days, into sharp-bordered, similarly-colored ulcers. The remaining portion of the palate still remains dark- red and swollen. The ulcers maintain their circumscribed con- tour, or in a few days involve the entire soft palate, not unfre- quently the mucous membrane of the cheeks also, as far as the lips, or the pharynx and upper portion of the larynx. They then diffuse a cadaverous or faecal odor, if they are not too small in extent. The disease is very painful. Swallowing and articu- lation are very much impeded, and may even be prevented. The submaxillary glands are usually considerably infiltrated, and frequently also the tissues adjoining them. The general symptoms are severe in both forms of gangrenous angina. The fever varies; the temperature may be normal, or slightly, or considerably, elevated ; the pulse is sometimes much retarded, at other times much accelerated. There is complete loss of appetite, frequently vomiting, etc. Consciousness may be maintained, or there may be a comatose condition. The course of the disease is acute. Limitation of the gan- grene, etc., occurs occasionally, and only in inflammatory gan- grene. In all other cases death takes place, usually in from four to ten days, in consequence of septicaemia, or hemorrhage from the diseased or other portions, or oedema of the glottis, or inflam- mation of the lungs, or, finally, from diseases which are con- nected with the primary disease, and not with the gangrene of the palate (inflammation of the kidneys in scarlatina, etc.). Gangrenous angina occurs most frequently in scarlatina. Its commencement presents nothing characteristic. There is usually, at first, an intense dark, somewhat livid reddening, fre- quently accompanied by hemorrhages and marked swelling of the soft palate and contiguous parts, as well as of the lymphatic glands of the jaw. The local manifestations are very prominent when they are not concealed by the severe general affection. To- wards the middle or end of the first week, less frequently during 966 WAGNER.—DISEASES OF THE SOFT PALATE. the second week of the disease, a dirty gray spot appears upon one tonsil or upon both. This usually extends rapidly, so that the entire soft palate becomes gangrenous in a few days. The termination is almost always fatal, usually under septic mani- festations. I have carefully examined two cases of this gangrenous angina pathologico- anatomically. One was fatal from the gangrene, the other from nephritis. On portions of the tonsils, which were intensely diphtheritic at the commencement of the disease, there lay deep, gaping furrows, the immediate surroundings of which were still gangrenous, while further outwards a dense, purulent infiltration existed in many places, a line or so in width, and reaching as far as into the muscular struc- ture. The contiguous portions of the palatine arches exhibited a slighter purulent infiltration. Pitha (Prag. Vtljschr. 1851. II. p. 27) and others describe an angina nosocomialis phagedmnica. It occurred during an epidemic of hospital gangrene, and affected patients with phagedenic ulceration, as well as individuals entirely healthy or in complete convalescence. It occurred suddenly, without assignable cause, for the most part over night. It involved the mucous membrane of the mouth, soft palate, and posterior walls of the nose. Grayish-white thick deposits occurred, underneath which the dark-red and acutely swollen mucous membrane underwent rapid destruction in from twelve to twenty-four hours, so that large lardaceous ulcers were formed with highly-reddened, jagged, and undermined edges. Consult also R. K. Browne (American Medical Times, Nov. 1862), concerning a characteristic gangrama faucium, a new form of hospital gangrene. It is probable that certain unclassified cases belong in this category, for example, Giinsburg (his own Zeitschrift. 1850. I. 2. H.): so-called pharyngo-typhus in a girl sixteen years of age; further, Guthrie (Edinb. Med. Jour. 1862. VIII. p. 297). Jobert (Ann. de ther. Mai, 1846) saw a case of perforation of the soft palate fol- lowing a wound from a crust of bread. Williams (Brit. Med. Jour. July, 1862) describes peculiar, perforating, non-syphilitic ulcers of the palate. Gangrenous angina has long been known. Its independent existence was denied in France by Bretonneau, who recognized it as a regular sequel of diphtheritic and scarlatinous angina; on the other hand, its independence was demonstrated later by Delaberge and Monneret (Compend. I. p. 134. 1836) ; "Rilliet and Barthez (Arch. gen. 1841. XII. p. 446); Guersent (Diet, en XXX. 1833. HI. p. 134); Trousseau (1. c.); and especially by Gubler (Arch. gen. Mai, 1857.) IV. Atrophy of the Palate, and especially of the Tonsils. Atrophy of the soft palate and atrophy of the tonsils some- times occur together, and sometimes the latter occurs alone. ATROPHY OF THE TONSILS. 967 Both affections have been practically but little investigated. The latter will almost exclusively occupy our consideration here. The causes of tliese atrophies are various. Congenital atrophy, deficient development of the tonsils, occurs not unfrequently. It consists in the tonsils and some- times the arches of the palate also remaining at a standstill, in the condition of early age. The tonsils are remarkably small, the number of the lacunae is usually small; they are shorter, and their surroundings exhibit smaller follicles, or the follicular arrangement of the cytogenetic tissue is wanting altogether. Atrophy from disease and from senile marasmus simultane- ously affects the tonsils and the soft palate, including the uvula. This atrophy occurs regularly in old age from well-known causes. The diseases in which it occurs are convalescence from severe acute diseases (typhus, etc.)—furthermore, chlorosis, tubercu- losis, diabetes mellitus, etc. In the diseases last mentioned the atrophy of the parts named is as regularly present as that of the entire body, and thus the soft palate becomes a true mirror of the general nutrition. The palate and the uvula are thinner, slender, and mostly very pale. The thinning affects the mucous membrane and the muscular layer; the mucous glands are sometimes diminished in size at the same time, and sometimes they project to a remarkable degree. The tonsils are small, the outlets of their lacunae are indistinct, their surface is level or slightly arched. Upon section they show especially a thinner, whiter, and firmer perilacunar tissue than natural, and poorer in cellular elements. Atrophy in consequence of operation, especially that of incomplete extirpation of the tonsils, is not always distinguish- able from the foregoing forms. Inflammatory atrophy of the tonsils occurs in a great number of persons. It occurs most frequently in both tonsils, in equal or unequal degree, less frequently in one tonsil only. It affects the tonsil either in its entire mass, or only in the upper or lower half, or only in its middle portion, or only in its length, breadth or thickness, or only the anterior or posterior half in its entire length, or only partially, or in still more limited extent. In this manner there occur a multitude of variations, most of 968 WAGNER.—DISEASES OF THE SOFT PALATE. which are not fully recognizable during life. A special descrip- tion of these variations is unnecessary. At the point of atrophy the tonsil is diminished to almost complete disappearance, in all its diameters, but especially in thickness. The cytogenetic tissue still remaining shows isolated follicles sometimes, but in most instances there is no longer any distinct follicular arrangement. Sometimes the reticular tissue is remarkably broad in its fibres, the interspaces being corre- spondingly small. (In individual cases large giant-cells with many nuclei were found in the atrophic cytogenetic tissue.) Sometimes the lymphatic vessels are remarkably distinct. The lacunae are mostly narrower, or they are obliterated in various places, and to a varying extent, most frequently on the free surface. Sometimes they are dilated in places, and filled with concentric layers of epithelium. The intermediate connective tissue is usually hypertrophied. The capsule of the tonsil is normal, or thickened in places or in its entire extent, most frequently on the surface. In the latter case fibrous processes usually pass from it into the interior of the tonsil. Sometimes the tonsil is composed in greatest part of connective tissue, which may be poor or rich in vessels, and is not unfrequently bestudded with minute masses of haematoidine. (In one case I found all the smallest arterial and venous vessels, as well as the capillaries, narrowed in calibre, their walls being ten times their normal thickness, and composed of a homogeneous, non-nucle- ated, amyloid-like substance.) Or it contains nuclei here and there, equally distributed between the fibres, or in process of gradual transformation into non-follicularly arranged cytogenetic tissue. This connective tissue, in many cases, contains fat cells in varying proportion, mostly irregularly distributed, seldom in lobular form. Near the base of the tonsil, more rarely at a dis- tance of from a half to two millimetres (T|¥ to yf^ of an inch) from the capsule, several elongated dense masses, either very small or barely visible, and composed of hyaline cartilage or of true bone tissue, are not unfrequently found lying in the connec- tive tissue. The muscular fibres on its external surface are some- 1 times to a great extent firmly adherent to the connective tissue.1 Concerning syphilitic atrophy, see further on. ATROPHY OF THE TONSILS. 969 Atrophy is frequently associated with dilatation of the lacuna, and they are filled with desquamated pavement epithelium, or at the same time with pus, or with the products of destruction of both, so that atheromatous, cholesteatomatous or abscess-like cavities are produced. The lacunae open either on the surface in the ordinary manner, or they are contract- ed in places—mostly near the surface—or they are entirely closed. Wlten the dilated lacuna open freely on the surface, they often reveal within them, and projecting beyond them to the size of a millet-seed and larger, grayish-yellow, dry masses which, after being removed spontaneously (by coughing, hawking, etc.), or artificially, are not unfrequently reproduced many times. This affection simulates most nearly the comedones of the external skin. This condition occurs sometimes in one only, sometimes in several, or nearly all the lacunae of one or both atrophied tonsils, and then excites one form of chronic angina. When the lacuna are closed at their orifices the condition of things is different. The number and size of the affected lacunae vary very much ; sometimes they are affected singly, sometimes in groups of from two to four, or even as many as ten. Their size varies from that of half a pea to that of two peas, and occasionally they may reach even that of a cherry. Their form is regularly round or elongated; less frequently irregularly jagged; in the latter instance the irregular shape is due either to the fact that lacunae of normal or slightly dilated calibre open into them, or to the fact that two or more neighboring lacunae have run together. If these are few and small, the size of the tonsil is not materially altered; in other cases, in spite of the atrophy, it may be of normal size or even larger. Some tonsils are almost entirely composed of such lacunae, and of the interme- diate atrophied cytogenetic, or almost pure fibrous tissue. The dilated lacunae sometimes lie near the surface of the tonsil, and sometimes deeper in its interior. In the former case, gray or yellowish, soft or tense, prominences form, covered with thin mucous membrane; these prominences are distinguished from abscesses chiefly by their long duration (they sometimes con- tinue for months), and the absence of any inflammation in the 970 WAGNER.—DISEASES OF THE SOFT PALATE. vicinity. In the latter case they are discovered only in the dead subject upon section. The contents of the lacunae are gray or grayish-yellow, or pure yellow. The consistence varies from that of thick gruel to that of milk ; it is uniform, or contains a variable number of round- ish lumps. The gray semi-fluid contents are composed principally or entirely of epithelium. This is arranged in layers, usually flat, less frequently in more globular form. The epithelium is often simply degenerated, less frequently in a state of fatty degenera- tion, sometimes with isolated larger, or numerous small vacuoles. The nuclei are single, sometimes multiple, normal or distended. Sometimes epithelial cells are found completely filled with pus corpuscles. The white, semi-fluid contents consist of pavement epithelium and crystals of cholesterine. The yellowish contents consist principally of pus corpuscles, which frequently exhibit different stages of fatty metamorphosis. The grayish-yellow, mortar-like contents likewise reveal epithelium filled with fine molecular masses of chalk, as well as larger but still microscopic globules of chalk, which sometimes adhere tightly to the inner surface of the lacunae. In all cases, bacteria appear in these contents, either mobile or immobile, punctiform, red-shaped, or thread-like in form, or we find shreds of shagreen-like masses of zoogloa. Many exceedingly small, brownish-yellow, curdy lumps, or even those as large as a millet-seed, consist almost entirely of these bodies. They lie free, or in the interior of the pavement epithelium. In two cases I saw mould-fungus in the lacunae, and several times fragments of food (vegetable-cell tissue, and striped muscular fibre). The lining of the lacunae is composed sometimes of only a few layers of pavement epithelium, sometimes of many (from ten to twenty) and is generally seated upon small, seldom upon hypertrophied papillae. The parts surrounding such lacunae are sometimes normal, sometimes compressed in various degrees, and atrophied ; in the latter instance, there is frequently no follicular arrangement. The reticulated tissue sometimes con- tains red or black pigment granules. Some lacunae, contracted or entirely closed superiorly, contain, alone or in connection with the contents described, one, and less frequently several concretions. These vary generally in size from that of a millet-seed to that of a pea; occasionally they are as large as cherries or even larger, of a brownish-gray color, round and smooth, or often irregularly indented (so-called mulberry calculi). They are principally composed of phosphate and car- ATROPHY OF THE TONSILS. 971 bonate of lime, and of a variable amount of organic material. The stones are either borne without further local disturbance, or they finally make their way to the surface, and are then usually coughed out. This takes place sometimes without severe inflam- matory and other symptoms, sometimes through the medium of a tonsillar or peritonsillar suppuration. Wurzer (Buchner's Rep. f. d. Pharm. XXIII. 2. H.) found in a tonsillar calculus removed during life 63.8 parts of phosphorus, 15.7 of carbonate of lime, 1 per cent. of iron, 7.1 of hydrochloric acid, soda, some potassa, and 13.3 of an animal matter. Robin found 50.0 of phosphorus, 12.5 of carbonate of lime, 25.0 of water, and 12.5 of mucus. Clinically, atrophy of the tonsils has received but little attention. It does no special damage in itself. In fact, many observations go to prove that persons with congenital or acquired atrophy of the tonsils are less subject to almost all the diseases of the tonsils, especially the ordinary inflammations, diphtheri- tis in its various forms, and syphilis. The dilatations of the lacunae (like comedones) have already been mentioned as a cause of chronic tonsillar angina. The cyst-like dilatations of the lacunae have a clinical importance in the fact that their con- tents act irritatingly on the contiguous parts, either mechani- cally or chemically. In this way are produced—and usually repeatedly—the various kinds of tonsillitis, and especially intra- tonsillar and peri-tonsillar abscesses. The latter condition is seldom demonstrable in the living subject. When, on the contrary, many tonsils are examined from the dead subject, and especially when, after previous hard- ening, several parallel sections are made through them, various far-reaching cicatrices, etc., are frequently found in the neigh- borhood of such cysts. Simultaneous atrophy of the soft palate and of the tonsils occurs not unfrequently in connection with chronic pharyngitis, especially with pharyngitis sicca. In what relation they stand to each other is for the most part unknown. Probably, however, the former in some cases is the predisposing cause of the latter. 972 WAGNER.—DISEASES OF THE SOFT PALATE. V. Hypertrophy of the Tonsils. Concerning the anatomical and histological relations, see Billroth, 1. c.— Virchow, Geschwulste. II. p. 609.-0. Weber, in Pitha-Billroth, Hdb. d. Chir. 1. c. p. 360.—Concerning the clinical relations, see Dupuytren, Repert. d'anat. et de phys. 1828. V.—Graves, Dubl. Journ. Jan. 1839.—Shaw, Med. Gaz. Oct. 1841. Bull de ther. May and July, 1843.—Robert, ibid.—Pitha, Prag. Vjschr. 1845. II.— Yearsley, On the enlarged tonsil, etc. 1848.—Roger, Semeiot. des mal. de l'enfance. 1864.—Desnos, in Nouv. diet, de med. et de chir. prat. 1865. II. p. 138.—The copious literature upon extirpation of the tonsils belongs to the domain of surgery. Hypertrophy of the tonsils is a true hypertrophy. All the constituents of the tonsil increase proportionately, the follicles especially becoming not only large, but also more numerous. It occurs in very different grades, less frequently in one tonsil only, oftener in both, and in the latter case to an equal or unequal degree. The size of the hypertrophied tonsil varies from a slight increase of volume to one the size of a walnut, and occasionally it reaches that of a small hen-egg. The tonsil retains its original form—only the prominences and depressions on its surface are more distinctly pronounced, occasionally to such a degree that the superficial surface becomes lobulated. Generally the entrances of the lacunae are larger and wider, cor- responding to the increase in size of the tonsil, and their already normally-arched contour is rendered still more distinct. The orifices may be empty, or filled with various substances. In most instances the position of the tonsil also becomes altered, as it becomes enlarged. Only occasionally does it remain lying chiefly between the palatine arches, so as to make them bulge forward at the corresponding point. In most instances it pro- trudes beyond its niche between the palatine folds towards the median line. At the same time it is usually somewhat lowered, rarely so much so as to appear pedunculated. In bilateral hypertrophy the pharyngeal vestibule is remarkably encroached upon, even so much so that only a small horizontal space remains between the root of the tongue and the soft palate. The uvula is pressed together from both sides, or it is often pushed backwards, or, less frequently, forwards. In HYPERTROPHY OF THE TONSILS. 973 extensive unilateral hypertrophy the uvula is pushed over to the opposite side ; it thus remains crooked, or is irregularly bent in various ways. Finally the middle pharyngeal space itself is narrowed by the corresponding projection of the hyper- trophied tonsils into this space. On section the hypertrophied tonsils are grayish-red, poor in blood, soft, but brittle, and homogeneous, with the exception of the fissures and their contents. The follicular arrangement on section of fresh tonsils is sometimes distinct and sometimes wanting. In the latter case it may be brought to view in the hardened tonsil, in thin sections, especially under a magnifying lens. The mouths of the lacunae will be found in a more or less gaping condition ; they are also wider and elongated in propor- tion to the increased thickness of the tonsil. They run vertically or obliquely into the tissue of the tonsil, and usually exhibit numerous prolongations. Around the lacunae are the follicles, increased in number even to the number of twelve on each side of the lacuna. They vary in size from £ to 2 mm. {^ to TV of an inch), and are mostly round ; but many of them are oval. They are usually distinctly separated from each other by interfol- licular tissue ; but not unfrequently two and even three of them lie so closely together that they appear as if formed by division, or some of them may be actually biscuit-shaped. Two follicles rarely lie the one upon the other. The larger follicles usually project somewhat into the interior of the lacuna. Microscopi- cally, the follicles and the reticulated tissue between them are essentially arranged as in the normal tonsil. The septa of con- nective tissue and the capsule are usually somewhat thickened. The superficial epithelium is of normal thickness or thicker, and the papillae beneath are usually increased in number, and some- times somewhat shorter. The epithelium, etc., of the lacunae present nothing characteristic. Hypertrophied tonsils so frequently exhibit all of the affec- tions already described, especially hyperaemia and the various inflammations, as well as partial atrophy, that these conditions, especially the inflammations, must be reckoned in the symptom- atology of tonsillar hypertrophy. The lymphatic glands of the jaw are often moderately enlarged, probably less as a result of 974 WAGNER.—DISEASES OF THE SOFT PALATE. the hypertrophy than of the subacute and chronic inflammation of the lacunae, etc. Sometimes most of the glands of the throat are larger and harder. * In hypertrophy of the tonsils the soft palate is either normal, or it exhibits chronic catarrh, and, with especial frequency, oedema of the uvula; or there is, at the same time, a slight hypertrophy of the mucous membrane, sometimes of the follicles also, and especially of the so-called auxiliary tonsils in the ante- rior palatine arches. Hypertrophy of the tonsils occurs frequently. It is encoun- tered mostly in the earlier years of life, and is then frequently inherited. In some families one of the parents and most of the children are thus affected. More rarely it occurs, for the first time, in the later years of childhood, and still more rarely after this period. It attacks both sexes with equal frequency. The special causes of hypertrophy of the tonsils are un- known. In one series of cases it is developed without attract- ing any notice and without any previous angina, and in these cases comes to the knowledge of the physician accidentally. According to some observers the influence of the first den- tition (from the sixth to the twenty-fourth month of life) is important. In a more frequent series of cases, the affected individual suffers repeatedly from catarrhal or parenchy- matous tonsillar angina; the swelling of the tonsil connected therewith subsides only incompletely, and after each attack the tonsils remain somewhat larger than before. The croupous, diphtheritic, and scarlatinous forms of angina, also, sometimes leave an enlargement of the tonsil after them. The symptoms of hypertrophy of the tonsils are local and general. They of course differ according to the grade of hyper- trophy, according to whether one or both tonsils are involved, etc. The local symptoms are in greater part readily explained on inspection of the entrance to the pharynx. Most of the pa- thologico-anatomical characters already described are easily recognizable. Sometimes the palatine arches are pushed for- 1 Consult Griesinger, Arch. f. phys. Heilk. IV. p. 515. HYPERTROPHY OF THE TONSILS. 975 ward to an abnormal degree. Only occasionally are they so broad that the hypertrophied tonsil cannot be seen by direct vision; in most instances the tonsils project far beyond them. The most striking appearance is the narrowing of the passage into the pharynx. The d/ifftculty of swallowing thus produced is sometimes slight and sometimes severe, and in either case is not always proportional to the degree of enlargement of the tonsil. It is never wanting in a high grade of the affection, but it is sometimes not perceptible to the patient, though distinct enough, usually, to objective observation. Breathing is much more affected; when very large tonsils perceptibly narrow the upper pharyngeal space, breathing is principally, or only, pos- sible through the mouth. The mouth is therefore always main- tained half-open, giving the patient a somewhat stupid look. The difficulty of breathing is slight in the erect posture, but on lying down, especially at night, it causes unquiet sleep, frequent outcries, sometimes symptoms similar to those of night-mare, or actual paroxysms of suffocation. Frequently there is loud snoring. Not infrequently the patient is often awakened at night by thirst, which is a result of keeping the mouth open. The speech, in high grades of hypertrophy, is less distinct, even nasal. The enunciation of I and r is especially indistinct (so- called paralalia literalis). Little children acquire speech with more difficulty. The range of the voice is usually circumscribed. The pitch of tone is, as a whole, elevated. Hearing is frequently affected, in consequence of pressure of the tonsil upon the pharyngeal extremity of the Eustachian tube, etc., but more so probably from extension of the catarrh of the mucous membrane (Harvey). The affection itself is altogether painless.1 A further series of local symptoms is only present at times. They are not consequent on the enlargement of the tonsil in itself, but upon the frequently coexisting catarrh, etc. Slight hemorrhages from the surface occur not unfrequently, especially at night; the patients expectorate buccal mucus mixed wdth blood. 1 Consult Bennati, Die physiol. u. path. Verh. d. menschl. Stimme. TJebers. 1833. [Recherches sur le mechanisme de la voix humaine; and Recherches sur les maladies qui affectent les organes de la voix humaine. Paris, 1832. ?—Tr.] 973 WAGNER.—DISEASES OF THE SOFT PALATE. The contents accumulating in the dilated lacunae, and decompos- ing there, sometimes produce a foul odor of the breath. This also often provokes the frequently recurring superficial or lacunal catarrh—the former sometimes resulting in an actual hypertrophy of the mucous membrane, the latter in purulent accumulations, etc. Extension of the hyperaemia into the nasal mucous mem- brane produces chronic coryza and frequent epistaxis in some individuals. Sometimes the catarrh extends regularly to the larynx, and there is hoarseness or obstinate cough. The disposition to croupous or diphtheritic angina is probably increased. In all diseases which are associated with enlargement of the tonsils, the local disturbances become greater. Severe grades of hypertrophy of the tonsils, when they occur in childhood, and when they are of long duration, sometimes exert an influence on the conformation of the countenance and, the thorax. The face does not grow in proportion to the remainder of the body, nor does the external nose ; the nostrils are frequently sunken in. The roof of the mouth also remains small, and is more strongly arched ; the upper alve- olar process of the upper jaw especially is very small, and in this way the space for the teeth in the upper jaw becomes nar- rowed, so that the anterior teeth especially assume an irregular position, and encroach in part upon one another. According to some, this deformity depends upon the diminished patulous- ness of the posterior nasal openings ; these and the contiguous structures remaining backward in development in consequence of lessened function (Robert). The deformity of the thorax varies. Most frequently it is compressed laterally in its inferior portion, the sternum is somewhat bulged forwards, and the verte- bral column is bent—similar to the pectus carinatum (Dupuy- tren). Less frequently the lateral walls of the thorax are more prominent, the breast-bone is depressed, and the vertebrae are little or not at all bent (Coulson, Warren). In both classes of cases the muscles of the chest are sometimes remarkably weak. Deformity of the thorax takes place after several years' continuance of the hypertrophy of the tonsils. It may disappear with the reduction in size or the extirpation of the tonsils, even when it has existed to a great degree (Shaw, Pitha, and others). Its cause is supposed to be the diminished entrance of air into the HYPERTROPHY OF THE TONSILS. 977 lungs, so that the external pressure of the atmosphere produces a compression of the thorax (Dupuytren, Shaw, and others). Robert compares the condition of the parts to a syringe whose walls offer but little resistance, and therefore, when the opening is small, sink in if the piston is suddenly withdrawn. In occasional cases there is almost continuous headache, in the forehead. The general system is almost always impaired in severe forms, and after the continuance for years of hypertrophy of the tonsils. The patients are usually pale and thin ; less frequently the face is somewhat puffy and slightly bluish. These manifestations, also, disappear quickly after the cure of the enlargement of the tonsils. Smith (Med. Times and Gaz. 1865. No. 786) refers to the danger of administer- ing chloroform in cases of hypertrophied tonsils. The course of tonsillar hypertrophy is always very chronic. The increasing hypertrophy may be arrested at any stage. This is the most frequent course. Or hypertrophied tonsils may gradually decrease in size, usually without special treatment— sometimes by the actual influence of gradual atrophy, as fre- quently occurs during puberty, or before it, or at a later age, sometimes under the influence of inflammatory atrophy. Finally, the tonsils may become so large, and the local and concomitant disturbances may become so important, that extirpation then becomes necessary. Treatment. No prophylactic measures are known which will prevent hypertrophy of the tonsils. Cold ablutions to the throat or the entire body, the former several times a day, and assiduous gar- gling with cold water, at least lessens the frequent recurrence of tonsillar catarrh, and thereby perhaps the increase in the hypertrophy also. For the latter condition itself all the various mouth-washes and gargles, the local applications of the various astringents by pencillings, etc., are probably without effect. The value of strong astringents and of superficial caustic reme- dies is also very questionable (nitrate of silver in solutions from VOL. VI.—62 978 WAGNER.—DISEASES OF THE SOFT PALATE. fifty grains to two drachms to the ounce, concentrated acids, caustic lime, tincture of iodine, etc.). I have seen at most super- ficial ulceration, but never an actual diminution of the tonsil, in cases of great hypertrophy, even after applications continued with regularity for months. The value of mud and sulphur baths, the latter much recommended by the French, is equally doubtful. Extirpation of the tonsils is to be undertaken in all cases where swallowing, breathing, or speaking is seriously impeded, where the hearing is affected, where deformity of the thorax is present, where the general condition is disturbed without any further apparent cause, and, finally, where frequent angina occurs, especially with a tendency to extension into the larynx. In many cases the extirpation of the inner half or a large por- tion of the tonsil suffices ; the remainder then performs its func- tions like a normal tonsil. Extirpation is also recommended by some observers during the existence of an acute tonsillar angina. Voltolini pierces the hypertrophic tonsil with the galvano-cautery. VI. Syphilis of the Soft Palate.' The soft palate is, next to the skin, the most frequent seat of syphilitic disease. This is very seldom primary, usually second- ary, less frequently tertiary. In reference to its method of appearance, etc., everything is true which is true of syphilitic affections in general. The following forms of syphilis of the palate are in many cases easy to recognize, and to differentiate from each other ; more rarely they merge into each other. Not unfrequently the physician is brought into contact only with the severer forms (and with these not until they have existed for a long time), especially among the poor, the previous conditions not having been attended to on account of the slight amount or total want of pain, difficulty of swallowing, etc. Syphilis of the palate usually affects both halves of the palate ■ For history and literature of syphilis of the palate, see Vol. III. of this cyclopaedia. SYPHILIS OF THE SOFT PALATE. 979 in equal or nearly equal degree, more rarely one side alone or to a greater degree. Most frequently it affects the surface of the tonsils, either alone or with the contiguous arches of the palate ; next in frequency comes the uvula, then the remainder of the soft palate with the palatine arches. 1. Syphilitic Erythema. Angina Syphilitica Erythematosa seu Catarrhalis. Catarrh frequently constitutes the first manifestation of secondary syphilitic disease of the mucous membrane, and also of the hereditary affection, but it usually produces such slight symptoms that it is not noticed by the patient. The catarrh usually involves the entire soft palate. It sometimes presents itself as an ordinary catarrh, sometimes with slight oedema, sometimes with the character of slight phlegmonous inflammation. It has no special characteristics from which the syphilitic nature of the affection can be recognized. Only its gradual commencement, its slight subjective disturbances, and its long duration, may excite suspicion. Sometimes fever exists at the same time. Frequently syphilis of the skin is present at the same time, in the form of roseola or papules. Syphilitic catarrh ceases of itself or after special medication, or it passes into the form next to be considered. Chronic syphilitic angina seldom results from the previous form, but oftener remains after the following form, especially in those who have been subject to anginas before contracting syph- ilis. It likewise presents nothing characteristic. 2. Syphilitic Alteration of the Epithelium. The under portion of the mucous membrane is generally diffusely, less frequently highly reddened, and probably always slightly infiltrated with cells ; the surface is colored whitish, over a varying extent and contour; it is slightly elevated, smooth, or slightly rough. This condition is found most fre- quently on the surface of the tonsils, and in their entire extent. The whitish coloration, according to preparations which I made 980 WAGNER.—DISEASES OF THE SOFT PALATE. in specimens taken from the living subject, is mostly due to a suppuration of the epithelium, less frequently to a true croup- ous metamorphosis of the epithelium. In the latter case the deposit is usually thicker, similar to that of non-specific pharyn- geal diphtheritis (see p. 954). In all other respects this form is similar to that previously described. 3. Syphilitic Papules and Patches. Angina Syphilitica Papulosa. Upon the mucous membrane, which is as a rule diffusely and moderately reddened, though sometimes entirely pale, are various prominences, frequently of the size of lentils, round or roundish, isolated or more frequently confluent, which depend upon a uniform small cellular infiltration of the mucous mem- brane, not unfrequently of the submucosa also, an cedematous condition of the latter being often also present at the same time. These elevations are always pale, mostly milk-white in color, and first catch the eye in consequence of this color. This appearance is produced by the cellular infiltration and anaemia of the mucous membrane. The surface of the elevations is sometimes smooth, sometimes rough, in the manner mentioned in section 2 (p. 979), and from the same causes there specified. This form of syphilitic angina comes most frequently under medical treatment, and may also be hereditary. The subjective disturbances are mostly moderate and similar to those of ordinary catarrhal angina. They vary according to the number and location of the diseased spots, and still more according to the severity of the catarrh of the non-papulous portions of the palate. Syphilitic patches dis- appear by absorption, after a variable length of time, either spontaneously or under the use of medicine ; or they ulcerate, superficially or to a variable depth. At the same time the same affection is frequently found at various portions of the mucous membrane of the mouth, on the inner surface of the lips, and at the corner of the mouth; and papulae, psoriasis, etc., may coexist upon the skin. SYPHILIS OF THE SOFT PALATE. 981 4. Syphilitic Nodes; Syphilitic Infiltration. Angina Syphili- tica Gummosa seu Parenchymatosa. Syphilitic patches pass in manifold ways into syphilitic nodes, or the latter exist as such from the beginning. There is then formed a roundish infiltration, mostly single, which may be as large as a cherry, and which undergoes destruction and ulcera- tion with tolerable rapidity. The contiguous parts are only moderately catarrhal. The disturbances are usually proportion- ately slight. Tliese nodes, according to their seat, either form a deep ulcer, or produce perforation of the palate, less frequently of one arch of the palate. Of especial importance and of tolerable frequency are the nodes developed on the posterior surface of the velum, mostly over the base of the uvula ; they often occur without being noticed, and are only to be suspected when ordi- nary examination of the palate shows collateral oedema of the parts. They speedily perforate the soft palate, not unfrequently with partial or complete detachment of the uvula. 5. Sypliilinc Ulcers. These may proceed from any one of the three last-mentioned forms. Those proceeding from the second form are erosions or shallow ulcers ; those from the third form are deeper, and like- wise the most frequent; those of the fourth form are the deepest, or they perforate the palate or the palatine arches, sometimes the tonsil also. These ulcers occur on any portion of the palate. Their size, number, configuration, etc., vary very much. Their floors exhibit the known peculiarities according to their age and stage of existence. These are not characteristics in themselves. An accurate diagnosis is only possible from the condition of the parts surrounding the ulcer, from the frequently simul- taneous existence of syphilitic alterations of epithelium or patches on the remaining portion of the palate, or in the cavity of the mouth, including the lips, and from the history of the case. Where tliese participations of the surrounding tissue, etc., are wanting ; where, also, catarrhal, phlegmonous, tuberculous, and other ulcers are apparently to be excluded ; where, finally, local 982 WAGNER.—DISEASES OF THE SOFT PALATE. treatment is unsuccessful, the diagnosis can only be made by the healing of the ulcers under the influence of anti-syphilitic treat: ment. The sufferings of the patient are those of an ordinary chronic catarrhal angina ; they are comparatively slight. JSTot unfrequently lack of cleanliness produces a foul breath. I have twice seen small, serpentine yellowish stripes, some of them as much as an inch in length, in the vicinity of rather deep syphilitic ulcers of the uvula and the contiguous palatine arches—apparently lymphatic vessels, filled with pus, or an affection of the parts surrounding the lymphatics. They disappeared at the same time that the ulcers healed. Syphilitic ulcers heal, when superficial, without leaving a cicatrix. The deeper ulcers heal under the formation of cicatrices (see section 6). 6. Syphilitic Cicatrices. Syphilitic cicatrices of the palate occur almost always after previous deep ulcers. They are found but very seldom without the simultaneous formation of ulcers. They possess no special characteristics. But as other sorts of deep cicatrices are very infrequent in the palate, we have the right to regard every large undoubted cicatrix in the palate, especially in its central portion, as of syphilitic origin, if there has been no operative process, or lupous affection, and if previous severe angina, especially that of scarlatina, has not existed. Syphilitic cicatrices occur in different forms, as follows : a. As thin milky spots, of varying size, most frequently on the surface of the tonsil; sometimes, also, on that of the con- tiguous palatine arches ; b. As deeper, whitish or yellowish-white spots, of varying size, which occupy either the largest portion of the palate, or only one portion of the middle third of the palate, or of the palatine arches, or the tonsils, or the uvula. The position of the adjoining portion of the palate is normal, or may be dis- torted in various ways; c. As perforations of the central portion of the palate, or of the palatine arches and tonsils ; d. As irregularly striped cicatrices of the palate, or as regular SYPHILIS OF THE SOFT PALATE. 983 or irregular lobulation of the tonsil. The first form corresponds to the deep cicatrices of gangrene of the external skin; the latter are analogous to the well-known lobulation of the surface of the liver and the infrequent lobulation of the tongue. Both of them, also, may be produced by syphilitic processes in the interior alone, without simultaneous syphilitic ulceration of the surface ; e. As distortions of the uvula from deep, but usually, at the same time, from superficial destructions, which leave weals behind them, analogous to those of the sterno-cleido-mastoid muscle, etc.; the uvula is bent forwards or backwards or to the side ; /. As syphilitic defects of the entire soft palate, or of only one-half, or of one palatine arch, and of the uvula in almost its entire length, or as syphilitic tonsillar atrophy ; g. As syphilitic adhesion of the palate to the posterior wall of the pharynx ; sometimes total ; either with the preservation of the uvula, and then, with absence of all communication between the upper and lower portions of the pharynx (that is to say, between nose and larynx), or after loss of the uvula, and then with slight, sometimes more extensive communication; at other times the adhesion is partial, the modifications in form, extent, locality, etc., being very various. The tonsils, whose surface is usually simultaneously affected in the above-mentioned forms, frequently exhibit alterations in their parenchyma, the amount of which does not always bear any relation to that at the surface. These are mostly wanting only in those instances in which the tonsil is in an advanced state of atrophy. These alterations are: hyperaemia, serous infiltration, parenchymatous inflammation, syphilitic infiltration, with consecutive ulceration or without it, and with lobulation of the surface. In the last instance the organ is composed almost entirely of connective tissue, traces only of the follicular tissue being still present. The immunity of the soft palate from syphilis in one of the forms mentioned, especially also from syphilitic cicatrices, while syphilitic affections show themselves in the lips, tongue, remaining mucous membrane of the mouth, and the pharynx, is more frequently met with in women than in men. The latter appear to be more disposed to syphilitic affections of the palate by indulgence in smoking, etc. 984 WAGNER.—DISEASES OF THE SOFT PALATE. Treatment. The treatment of syphilitic affections of the palate is both local and general. The local treatment consists in abstinence from injurious practices (the use of irritating food and drink, smoking, etc.), and in the employment of cleansing or disinfec- tant astringent mouth-washes, gargles, etc. The general treat- ment is the well-known mercurial treatment. VII. Morbid Growths of the Soft Palate. Concerning hypertrophy, of the tonsils especially, and con- cerning syphilitic morbid formations, see pp. 972 and 978. Besides those mentioned, almost all the morbid growths known are observed on the palate, a circumstance readily explained by the multiplicity of the tissues of which it is composed, and the various injurious influences to which it is subject. The morbid formations are primary, or secondary— extensions from contiguous tissues. They are circumscribed or diffuse. Some of them are altogether unimportant or especially of surgical interest. Others, on the contrary, especially those which are diffuse, are particularly of clinical interest. Most of the latter pass into ulceration, and frequently first come under observation in this stage. Neoplasms of the soft palate are not frequent, if we except hypertrophy and syphilis, and are little known clinically or pathologico-anatomically. In what follows, only those which interest the medical practitioner will be more particularly described. Clinically considered, morbid growths are important, by their local action in impeding swallowing, etc.; by their extension upon the contiguous parts ; and by the fact, peculiar to some of them, of simultaneous occurrences taking place in other organs and tis- sues. Etiologically, nothing is known concerning them. Thera- peutically, internal medication is entirely fruitless ; surgical as- sistance only is indicated ^extirpation, hot-iron, galvano-oautery). 1 Consult Passaquay, Tumeurs des Amygdales. Paris. 1873. MORBID GROWrTIIS. 983 1. Neoplasms of Connective Tissue and Vessels, of Fatty Tissue, and of Muscular Tissue. Diffuse connective-tissue new formations, in the form of hypertrophy, either of the uvula alone, or of the entire soft palate, and sometimes, also, of the tongue, etc., have occa- sionalty been observed in entirely healthy subjects, as w~ell as in cretins. But they are very rare, and are almost always con- genital. Very rarely fibromas occur in the form of small tumors in the palate and in the tonsils.1 Myomas likewise occur very seldom. I have seen one small flattened myoma, the size of a small pea (myoma strio- cellulare), sharply circumscribed, in the submucosa of the posterior surface of the soft palate. Lipomas are also infrequent. Lambl (Aus. d. Franz-Josef-Kinderspit 1860, p. 181) describes a pedunculated lipoma the siza of a pear, lipoma pharyngis cum indumento dermoidali, which probably sprung from the posterior surface of the palate of a female child six months of age, and which became detached spontaneously. Primary sarcomas appear to be exceedingly infrequent in the soft palate. Somewhat more frequently they spread from the contiguous tissue, especially from the fissures and cavities of the neighborhood on to the lateral portions of the palate. Papillomas possess characteristics sometimes more like those of warts, sometimes more like those of a chondyloma. They are the most frequent of the circumscribed morbid growths, usually smaller than peas, seldom larger, and have broad or narrow pedicles. Their favorite seat is on the uvula ; they are less fre- quent on the remaining portions of the soft palate and on the tonsils. Most frequently they exhibit no symptoms of their existence; occasionally they give rise to slight symptoms, and still less frequently to severe symptoms.2 1 Curling, The Lancet. 1858. No. 6. 8 Consult the case of Ilerzfelder (Wbl. d. Z. d. Wien. Aerzte. 1856. No. 30), in which hysterico-epileptic convulsions always set in on lying down, in a patient nineteen years of age. After extirpation these symptoms disappeared. 986 WAGNER.—DISEASES OF THE SOFT PALATE. 2. Lymphatic Morbid Formations. In typhoid fever new formations, similar to those occurring in the bowels, etc., occur but very unfrequently.1 In leukamia, the lienteric as well as the lymphatic form, lymphomas sometimes occur in the mucous membrane of the soft palate and the pharynx ; the tonsils are transformed into medullary tumors of different sizes. These conditions, when strongly developed, are visible during life.2 In lepra similar nodes occur on the palate, etc., as on the skin. Lupus of the soft palate occurs almost always simulta- neously with lupus of the nose or of the face. It sometimes affects the palate only, sometimes the pharynx and upper por- tion of the larynx at the same time. It usually has the form of lupus exulcerans, and then either proceeds to cicatrization without great loss of substance, or it may destroy the palate in varying extent, after which, likewise, cicatrization or adhesion to the posterior wall of the pharynx, etc., may ensue. The treatment is similar to that for lupus of the skin. Simultaneous lupus of the face and of the palate is not infrequent. The mucous membrane of the mouth may be normal, or there may be lupous morbid growths upon the lips and the gums. When lupus affects the palate alone, its differentia- tion from some syphilitic infiltrations and ulcers is the more difficult, because some forms of lupus are without doubt of syphilitic nature ; at least they heal promptly under the use of mercury and iodine, even when they have existed for months and years. The cicatrices of healed lupus are characteristically striated like those of the external skin. The tonsils, in such cases, are often hypertrophic. Tuberculosis of the soft palate occurs only simultaneously with advanced tuberculosis of other organs, especially of the lungs, usually of the larynx also, especially its upper portion, of the root of the tongue, and of the pharynx. At first there is 1 Concerning the alterations in the tonsils in typhoid fever, hypertrophy of the follicles, etc., see C. E. E. Hoffmann, Unt. iib. d. pathanat. Veriind. der Org. beim Abdominal typhus. 1869. p. 158. 2 Consult Mosler, Virch. Arch. 1868. XLII. p. 444.— Idem, Die Leukamie, 1872, p. 181.— Valtat, in Passaquay, 1. c. p. 41. The tonsils healed similarly in a case of lienteric and at the same time lymphatic leukaemia that I observed myself. MORBID GROWTHS. 987 a tolerably uniform thickening and infiltration of the mucosa and submucosa, usually of the entire soft palate, frequently including the tonsils. This renders the surface pale. Fre- quently a suppuration of the epithelium occurs, which gives the surface an appearance similar to that of a flat croup deposit. Tuberculous masses, from the smallest size to that of peas, occur but seldom in addition to the uniform flat infiltration. Further- more, numerous shallow ulcers usually occur, which coalesce at a later period, and produce fissures of various depths on the surface of the tonsils. It seldom amounts to extensive and deep ulceration in the soft palate, while tliese conditions are more frequent in the pharynx. The lymphatic glands of the jaw are likewise tuberculously infiltrated, but generally only to a slight degree. Microscopically tuberculosis of the palate exhibits nothing special. The deeper tuberculous ulcers almost always show the muscles likewise infiltrated with tubercles. Clinically the diagnosis is easy, from the symptoms men- tioned, and from the existence of extensive tuberculosis of the lungs, etc. The disease is most frequently confounded with some syphilitic affection of the palate. The variation in the painful- ness of the two is also common to both classes of affections, only tuberculosis appears to be painful more frequently than syphilis, and sometimes causes very serious difficulty in swallowing. Tuberculosis of the palate is much less rare than one would surmise from the sparse pathologico-anatomical and clinical descriptions. Consult Weber, in Pitha, Billroth's Chir. 1866. III. 1. Abth. pp. 337 and 360.—B. Wagner, Arch. d. Heilk. 1865. VI. p. 470.— E. Wagner, ibid. 1870. XII. p. 5.—Ouhnont, Gaz. des Hop. 1S66. No. 43.— Trclat, Arch. gen. Jan. 1870. The so-called scrofulous ulcers of the palate and pharynx, angina scrofulosa, are not yet sufficiently studied to admit of any general exposition. The cases referred to this category, which usually affect the pharynx at the same time and to a greater degree, are perhaps real scrofulous ulcerations similar to those of the skin ; or they are secondary, or extensions of pre- vious tuberculous ulcerations, or they have a lupous, leprous, or syphilitic character.1 1 Consult Hamilton, Dublin Journ. 1815. XXVI. p. 2S2.—Isambert, Gaz. hebd. 1871, No. 47. L Union. Nos. 3-6. 988 WAGNER.—DISEASES OF THE SOFT PALATE. 3. Epithelial Morbid Formations. Epithelial thickenings (so-called psoriasis oris) on the surface of the tongue, on the lips, and on the inner surface of the cheeks, occur most frequently in habitual smokers, occasionally as the result of other causes, or even in women. I have only seen them on the most anterior portion of the soft palate and simultaneously upon the hard palate also, but always only to a very slight extent. In those cases which I saw, the same affection existed at the time upon the skin of the hands, nose, and ears, and showed an inclination partly to the forma- tion of crusts and partly to the development of callosities or warts. In the palate they were regularly pierced by the mouths of the mucous glands. Mucous polypi, adenomas, are likewise very seldom found in the soft palate, and then most frequently on its borders as well as at the base of the uvula. They are usually single, seldom double, and when double they are sometimes symmetrical, with a broad base, more rarely pedunculated, and of a size which may reach that of a walnut or even a hen's egg. They have the known characters of these tumors, and sometimes contain cysts in places ; sometimes they contain smaller or larger calculi. They occur more frequently in youthful subjects. I saw one tumor, the size of two peas, in a child three weeks of age.1 4. Cancer. Cancer of the soft palate and of the tonsil occurs but rarely. The most frequent method of its occurrence is by spreading from contiguous parts ; it is more rarely primary, and most rarely secondary, appearing then in the form of one or more little nodules. Cancer may extend upon the palate from all portions of the surrounding structures, most frequently from the base of the tongue and from the pharynx, less frequently from the 1 Consult Rennes and Robin, Gaz. des Hop. 1855. No. 41.—NeLaton and Robin, ib. 1856. No. 143.—Anselmier, L'Union. 1856. No. 128.—Langenbeck, Deutsches Klinik. 1859. No. 48. ORBID GROWTHS. 989 larynx, the mucous membranes of the cheeks, the nose, the parotid gland, and the base of the skull. Primary cancer occurs more frequently in the tonsils than in the other portions of the soft palate. Both primary cancers and cancers from extension are most frequently epithelial in character, less frequently of the soft connective tissue variety (so-called encephaloid). The first occur almost exclusively in elderly persons; the latter at all ages, often in young subjects. The first give rise in general to slighter infiltrations, and usually have a slower course; they are sometimes very markedly papillary. The latter usually form larger, rapidly-growing tumors, more frequently starting from the tonsils. Both forms are greatly disposed to ulcera- tion. Secondary cancer of the palate, under certain circumstances. may be of diagnostic interest. I once saw small secondary nodules in the closed follicles of one palatine arch and the root of the tongue in a case of primary encephaloid of the root of the lung. Some diffuse morbid growths in the palate and pharynx, re- cently described as lymphoma, tymphadenoma, etc., are enceph- aloid. The diagnosis of cancer is usually easy, because it does not often come under observation in its earlier stages. The most important diagnostic indications are : the presence of a new for- mation, which extends upon all the surrounding parts ; its slow course, as compared with that of an inflammation ; its ulcera- tion with or without previous or simultaneous hemorrhage ; and the usual existence of swelling of the lymphatic glands of the jaw. The local disturbances are very various, according to the extent and volume of the cancer, but are not distinguishable from those dependent on ordinary causes. The affection may be altogether painless. The general symptoms vary according to the nature of the local symptoms, the existence of hemorrhage, the extension upon contiguous organs, etc. The regular termination is in death; usually by starvation, 990 W^AGNER.—DISEASES OF THE SOFT PALATE. hemorrhage, suffocation, etc.; less frequently by secondary cancer.1 5. Cysts. Cysts of the palate are mostly retention cysts, rarely new formations. They originate but rarely in the mucous glands, and may form circumscribed tumors reaching the size of cherries, similar to the like occurrences in the lips. They take their origin much more frequently in the lacunae of the tonsils, and then usually have the characters of atheromas (see p. 969). A new formation of cysts is very infrequent. In a women eighty years of age, I saw on the posterior surface of the soft palate above the uvula, a cyst the size of a half pea, with fatty, curdy contents, enveloped with a single layer of ciliated epithelium. Echinococcus has been observed in the palate only a few times. VIII Nervous Affections of the Soft Palate. The nervous affections of the palate will only be treated of concisely here, because they will receive a detailed consideration in a later volume of this series. They affect mobility, sensibil- ity, and nutrition. 1. MOTOR DISTURBANCES. A. Paralysis of the soft palate. Paralysis of the muscles of the soft palate either occurs alone, or simultaneously with paralysis of other muscles, most fre- quently those supplied by the facial nerve. There may be central paralysis, paralysis of conduction, or peripheral paralysis. Paralysis following diphtheria, the form most frequently en- countered, probably belongs to the latter class. It may be com- plete or incomplete (paralysis or paresis). It may be simple or 1 0. Weber, Chir. Beob. p. 364.—Poland, Brit, and For. Med.-Chir. Rev. 1872. XLIX. p. 477. NEUROSES. 991 associated with disturbance of sensibility or of nutrition. The paralyses occurring simultaneously with catarrh, phlegmonous inflammation, morbid growths, etc., are thrown out of considera- tion here. a. Isolated paralysis of the palate may affect individual muscles only, or all the muscles collectively. a. Paralysis of the azygos uvulce muscle may be unilateral or bilateral. In unilateral paralysis the uvula is bent towards the opposite side. Swallowing and speaking are not impeded. In bilateral paralysis the uvula is elongated, and cannot be retracted spontaneously nor by local irritation (touching it, etc.). Deglutition and articulation are not impeded. When the uvula is so long that it touches the root of the tongue, in the standing and sitting postures, involuntary movements of deglutition occur not unfrequently. If it touches the posterior wTall of the pharynx, adhering to it at times, frequent hawking is produced. Paralysis of the uvula alone has no significance in determin- ing the seat of the nervous disease. A distortion and an elongation of the uvula, with slight power of retraction, or none at all, also occurs very frequently after repeated anginas, in chronic angina, as a consequence of cicatrization, etc. /8. The levator and the tensor veli palatini muscles are almost always paralyzed simultaneously, and almost always both sides are affected—sometimes, however, in unequal degrees. The soft palate is depressed to a varying degree, and appears relaxed ; it is but little or not at all elevated in breathing. If the soft palate, the uvula especially, is touched, no move- ment is produced in pure cases of complete paralysis. If the tensor is not completely paralyzed, the palate is made some- what tense, but is not raised. It is usually drawn somewhat downwards and backwards by the pharyngo-palatine muscles. Swallowing is impaired to a high degree; the food taken, espe- cially if liquid, is regurgitated in greater part through the nose ; but not completely, if the superior constrictor muscle of the pharynx remains normal. Speech is nasal, indistinct, especially in the palate sounds. Sucking, gargling, blowing a light out, and forcible distention of the cheeks, are impossible. 992 WAGNER.—DISEASES OF THE SOFT PALATE. 7. Paralysis of the pharyngo-palatine muscles occurs ex- tremely seldom as an independent affection. In one case of Duchenne's, irritation of the uvula did not produce any mutual approximation of the posterior palatine arches, and no formation of a division-wall between the upper and middle portions of the cavity of the pharynx. Swallowing was somewhat impeded, but speech was not implicated. Paralysis of the glosso-palatine muscles has not been ob- served as an independent affection. S. Paralysis of the muscles of the soft palate collectively often occurs. The soft palate is depressed, and does not move in breathing or on local contact with a foreign body. Swallow- ing is very difficult, or altogether impossible, etc.; all the other relations are the same as those mentioned under the headings a, j3, and 7. b. Paralysis of the muscles of the palate and of other muscles. a. Simultaneous paralysis of the palate and of the facial muscles. The causes of this affection reside in the nervous centres (the hemispheres, the pons, and most frequently the medulla oblongata), or in the course of the facial nerve (caries of the temporal bone, pressure of the forceps in artificial delivery), or in the periphery (rheumatic and traumatic causes), or they are un- known (diphtheritic paralysis). The paralysis is almost always unilateral, extremely seldom bilateral. It most frequently affects one-half of the uvula, and one levator veli palatini. In slight cases the uvula is normal, or it moves on contact towards the healthy side only; the palatine arch is somewhat flatter. In more pronounced cases the uvula is drawn towards the sound side, and the palate hangs lower. (Various observations, differ- ing from tliese, may be found elsewhere.) /3. Simultaneous paralysis of the palate and the correspond- ing half of the body occurs in some cases of hemiplegia from cerebral hemorrhages, etc. 7. Simultaneous paralysis of the palate and the motor por- tion of the trifacial nerve affects the tensor veli palatini and one or more of the muscles of mastication. The cause is usually central. NEUROSES. 993 8. Paralysis of the palate in progressive glosso-pharyngo- labial paralysis is usually but little pronounced, so far as can be ascertained by inspection, but is more strongly indicated by destruction of function. e. Paralysis of the palate in progressive muscular atrophy. X. Paralysis of the palate in acute ascending paralysis (Landry). B. Spasm of the soft palate. Spasm of the soft palate is almost entirely unknown. Even the behavior of the affected muscles in spasms proceeding from the facial nerve, and in those proceeding from the motor fila- ments of the tri-facial, is unknown. In advanced cases of paralysis agitans movements occur in the soft palate similar to those in the muscles of the exterior. In a patient, with constitutional syphilis and paralysis of one-half of the body (without involvement of the palate), I saw twitching movements, synchronous with the pulse, in the left and sound half of the palate. 2. SENSORY DISTURBANCES. Anasthesia of the soft palate, mostly with diminished reflex irritability, is found in insane patients, and also in consequence of the influence of some substances upon the peripher}*- (ice, bromide of potassium, morphine, lye, etc.). In diphtheritic paralysis there is almost always paralysis of sensation likewise. Hyperasthesia of the soft palate occurs as well with the maintenance of a normal appearance of the parts, as in the various disturbances of circulation and the inflammations. Char- acteristic neuralgias, analogous to those of other branches of the trigeminus, have not been accurately observed. Tiirck (Wien. allg. med. Ztg. 1862. VII. No. 9) describes a neuralgia and hyperesthesia of the pharyngeal entrance; his description is based upon some six cases (two in males, four in females), most of them unilateral, but always more severe on one side. The symptoms were various—sometimes very severe pains, at other times only difficulty in swallowing, a sensation as of a tumor or foreign body, or of dryness in the parts. The duration varied from six weeks to six years. Treatment: Cauterization with nitrate of silver; resection of the lingual nerve. VOL. VI.—63 994 WAGNER.—DISEASES OF THE SOFT PALATE. 3. DISTURBANCES OF NUTRITION. These are still less known than the disturbances of sensation. The palate and uvula are sometimes atrophic in hemiatropliia facialis, which mostly affects the left side of the face. Appendix. Diseases of the muscles of the soft palate alone are not known. Where they occur simultaneously with diseases of other muscles or of all the muscles of the body, i. e., in the fatty metamorphosis from poisoning by phosphorus, etc., and in the trichinous disease, the participation of the palate is devoid of practical interest. INDEX. Abeille, 963. Aberle, 681, 684. Abscess in acute diphtheritic endocarditis, 66. Abscess of heart. See Myocarditis. Acetate of lead in aneurism, 459; in cerebral aneur- ism, 443 ; of potash in pericarditis, 619; in val- vular diseases, 169. Acid, benzoic, in whooping-cough, 727; carbolic, in stomatitis catarrhalis, 769; gallic in chyluria, 543 ; hydrochloric, in noma, 816 ; hydrocyanic. in whooping-cough, 726 ; in nervous palpitation of heart, 307; mineral, in acute diphtheritic en- docarditis, 80 ; nitric, in nomn, 816 ; in whoop- ing-cough, 727 ; pyroligneous, in noma, 816; salicylic, in diphtheritic endocarditis, 80 ; sul- phuric, in noma, 816 ; tannic, in aneurism, 459; in whooping-cough, 727. Ackermann, 219. Actual cautery in noma, 817. Acute yellow atrophy of liver in etiology of fatty de- generation, 250. Adams, 727. Adrian, 962. Age, influence of, in etiology of acute diphtheritic en- docarditis, 72; of acute myocarditis, 227; of aneurism, 415 ; of cancer of the tongue, 752; in chronic aneurism, 245; of chronic endarteritis, 375; of chronic myocarditis, 239; of contracting and sclerotic endocarditis, 99 ; of hypertrophy of heart, 199; of insufficiency of the pulmonary valves, 153; of insufficiency of the tricuspid valve, 147; of pericarditis, 560 ; of spontaneous rupture of heart, 263; of stenosis of the pulmonary os- tium, 155 ; of stenosis of the right ostium venosum, 150; of subacute verrucose endocarditis, 85 ; of whooping-cough, 685 ; influence of, in inspection of heart impulse, 22 ; on frequency of tendinous Bpots on pericardium, 550 ; on position of heart, 176; in prognosis of insufficiency of the mitral valve, 125; of pericarditis, 616; of whooping- cough, 716. Air, compressed, respiration of in treatment of val- vular diseases, 170. Aitken, 376. Albers, 286, 287, 958. Alberti, 680. Albertini, 61, 62, 189, 458, 548. Albuminuria in acute myocarditis, 236; in congenital diseases of the heart, 328; in insufficiency of the aortic valves, 140 ; in pericardial adhesions, 636 ; in subacute verrucose endocarditis, 89 ; in valvu lar heart disease, 113; in whooping-cough, 707. Albutt, 99, 395, 412, 622. Alcoholism in etiology of aneurism, 416 ; of chronic endarteritis, 375 ; of fatty degeneration, 248 . of contracting and sclerotic endocarditis, 99. Almond shells, sweet, decoction of, in whooping- cough, 727. Alter, 523, 528. Alquie, 858. Ammonias, aqua, in whooping-cough, 727; carbonate of, in acute diphtheritic endocarditis, 81; in treatment of heart clots, 297. Ammonium, bromide of, in whooping-cough, 727. Amussat, 410. Amyl, nitrite of, in valvular diseases, 172. Anaemia in etiology of fatty degeneration, 249; of the brain in stenosis of the ostium aorticum, 145. Anatomy and position of the heart, 7. Anderson, 493. Anderson, McCall, 393. Andral, 63, 225, 375, 520, 521, 522, 530. Aneurisms, saccular, at base of brain in valvular heart disease, 116. Antimony in noma, 816: in whooping-cough, 721. Aorta ascendens, its situation, 10. Aorta, narrowing of, in etiology of hypertrophy of heart, 192. Aortic valve, insufficiency of, in etiology of hypertro- phy of heart, 194. Aperients in valvular diseases. 168. Apoplexy in insufficiency of the mitral valve, 124. Aran, 263. 622, 629. Armauer-Hansen, 522. Armstrong, 7 Arnold, 747. Arterial foramina, their situation, 9. 996 INDEX. Arteries, Diseases of the, 345; bibliography, 345. Inflammation op the External Arterial Coat, Arteritis Externa, Exarteritis, Peri- arteritis, 346 ; bibliography, 346; pathology, 346; etiology, 347; symptoms and course. 348; treatment, 348 ; periarteritis nodosa, 349; arterio- capillary fibrosis, 350. Disease of the Middle Coat of the Arteries, 350; pathology, 351; fatty and calcareous de- generation, 351; diagnosis, 352; atrophy of the middle coat, 352; hypertrophy of the media, 354; prognosis, 355; treatment, 355. Spasm and Paralysis of the Middle Coat of the arteries, 356; etiology, 356; symptoma- tology, 357; treatment, 361. Acute Endarteritis, 362; bibliography, 362; pathology, 362; the lining epithelium, 363; etiology, 363; symptomatology, 365; treatment, 365. Chronic Endarteritis, Endarteritis Defor- mans seu Nodosa of Virchow. Arterio-sclerosis of Lobstein. Atheromatous Process of Forster. Atherosis, Induration of the Arteries, 366; bib- liography, 366: pathology, 366 ; the calcareous de- generation, 369; fatty degeneration of the intima, 370 ; results of chronic endarteritis upon external condition of the arteries, 371; mode of occur- rence, 374 ; etiology, 375 ; symptomatology, 377; dilatation and hypertrophy of the heart, 378; affections of the valvular apparatus, 379; the pulse, 380 ; gangrene following the disease, 383 ; oedema and varicose veins, 383; brain symptoms, 384; those of other organs, 384; course of the disease, 385; treatment, 386. Hypertrophy of the Arterial Coats, 386; pathology, 387; measurement of different arter- ies, 38S. Atrophy of the Arterial Coats, 390; pathology, 390. Degenerations, Neoplasmata of the Arterial Walls, 390 ; fatty degeneration, 390 , calcifica- tion, 391; amyloid degeneration, 391 ; carcino- ma. 391; parasites, 393. Syphilitic Diseases of the Arteries, 394; bibliography, 394; pathology, 394 ; diagnosis, 397; symptomatology, 397 ; duration of the dis- ease, 398; treatment, 398. General Dilatation of the Arteries, 398; bibliography, 398; measurements of diameter, 398; etiology, 400 ; symptomatology, 402; treat- ment, 404. Aneurism, 405; bibliography, 405; anatomy, 306; etiology, 410 ; disease of the coats, 410; position and ratio of occurrence as to occupation and sex, 414; symptomatology, 416; aneurism of the aorta, particularly of the thoracic aorta, 417 ; the impulse, 417 ; percussion, 418 ; auscultation, 419; the pulse, 422 ; pain, 425 ; the respiration, 425; disturbances of deglutition, 426; other symptoms, 427; rupture, 427; aneurisms of the ascending portion of the aorta, 429 ; per- cussion and auscultation, 429; the pulse, 431; other symptoms, 431 ; rupture, 431 ; aneu- risms of the transverse portion of the arch of the aorta, 432; aneurism of the descending thoracic aorta, 433 ; aneurisms of the innomi- nate, carotid and subclavian arteries, 434 ; aneu- rism of the pulmonary artery, 435; bibliography, 435; aneurisms of the ductus Botalli, 436; an- eurism of the abdominal aorta, 436; bibliog- raphy, 436; symptomatology, 437; aneurisms of other arteries in the abdomen, 439 ; aneurism of the cerebral arteries, 440 ; bibliography, 440 ; symptomatology, 441; diagnosis, 442 ; prognosis and treatment, 443; multiple uneurisms, 443; diagtiosis, 444; course and result, 447; progno- sis, 449 ; treatment, 449 ; bibliography, 449 ; ligature, 451: compression, 452; subcutaneous injection of ergotine, 453; injections into the aneurismal cavity, 454; introduction of foreign bodies, 454; galvano-puncture, 455 ; general treatment, 458; diet, 458; rest, 458; internal remedies, 459; symptomatic treatment, 460. Narrowing of the Arteries, 463; bibliography, 463; congenital uniform stenosis of the aorta and its branches, 464; pathology, 464; etiology, 465; symptomatology, 466; diagnosis, 469; prognosis and course and treatment, 470; lo- cal contraction and obliteration of the ar- teries, 471; bibliography, 471; etiology, pa- thology, symptomatology, and results, 471; contraction and obliteration of the aorta at the junction of the ductus Botalli, 473; pathology, 473 ; symptomatology, 475; prog?iosis and treat- ment, 476 ; narroioing of the aorta in ascending portion from external pressure, 477; of other arteries, 478; narroioing and occlusion of the pulmonary artery, 479. Rupture and Perforation of the Arteries. Dissecting Aneurism, 480 ; bibliography, 480; etiology, 481; symptomatology, 484 ; treatment, 485. Artery, pulmonary, affections of in etiology of hyper- trophy of heart, 196,197. Arteries, measurements of, 388, 398. Assafoetida in whooping-cough, 727. Atelectasis in whooping-cough, 704. Atheroma in etiology of atrophy of heart, 221 : of pulmonary artery in etiology of hypertrophy of heart, 197. INDEX. 997 Atropine in whooping-cough, 726. Auenbrugger, 62, 189, 548. 582. Aufrecht, 522. Auricle, left, its situation, 9; right, its situation, 8. Auscultation in aneurism of aorta, 419, 429 ; in acute myocarditis, 233 ; in chronic endarteritis, 378; in congenital diseases of the heart, 328 ; in congeni- tal narrowing of the aorta, 407 ; in dilatation of heart, 212; in examination of heart, 25, 48 ; in fatty degeneration of heart, 255; in insufficiency of the aortic valves, 135; in insufficiency of the mitral valve, 121; in insufficiency of the pul- monary valves, 154 ; in insufficiency of the tricus- pid valve, 148; in local narrowing of arteries, 472; in narrowing of the aorta, 475; in narrow- ing of the pulmonary artery, 479 ; in nervous pal- pitation, 304 ; in stenosis of left ostium venosum, 127; in stenosis of the ostium aorticum, 144; in Btenosis of the pulmonary ostium, 157 ; in sten- osis of the right ostium venosum, 151; in whoop- ing-cough, 696; in wounds of heart, 278. Autenrieth, 709. Axenfeld, 477. Ayres, 630. Baccelli, 454. Baeumler, 46, 603, 604, 570, 573, 654. Baillie, 550, 638. Baillou, 679. Baler, 642. Balfour, 404, 460, 468. Ballantyne, 726. Baly, 549. Bamberger, 15, 16, 20, 22, 33, 35, 36, 63, 85, 143, 149, 178, 179, 206, 211, 347, 375, 380, 409, 412, 432, 460, 467, 555, 583, 597, 615, 619, 632, 659, 665, 668, 787, 808, 853, 858. Barascut, 895. Barbette, 896. Barbier, 272. Barbosa, 962. Baerensprung, 905. Barlow, 630, 672 Baron, 816. Bartels, 957, 959, 961. Barth, 261, 263, 265. Barthez, &5, 581, 630, 681, 685, 688, 700, 702, 713, 724, 725, 813, S40, 966. Bartlett, T. H., 622. Bastian, 522. Baths in subacute verrucose endocarditis, 92; in val- vular diseases, 166. Battus, 808. Bauer on disease of the pericardium, 547. Baur, 209. Beale, 539. Beau, 169, 630, 681, 690, 709. Becker, 138, 264, 425, 659. Beckman, 193. Bednar, 685, 727. Beer, 264. Behr, 832. Bekman, 68, 112. Bell, Benjamin, 269. Belladonna in treatment of valvular diseases, 167 ; in whooping-cough, 721, 726. Bellingham, 420, 459. Benedict, 155, 826. Beneke, 167, 400, 409. Benivenius, 225, 292. Bennet, 428, 529. Benoit, 702. Benzoic acid in whooping-cough, 727. Berger, 686, 727. Bergeron, 720, 782, 895. de Berghes, 273. Bergmann, 797. Berlinerblau, F., 360. Bernard, Claude, 360. Bernstein, 300. Berthold, 245. Bertin, 189. von Bezold, 29S, 299, 300. Biborate of soda in thrush, 806. Bicuspid valve, its situation, 9. Bidder, 798. Biermer, 249, 680, 682, 685, 699, 700, 702, 715. 725. Biesiadecki, 735. Billard, 288, 630, 816. Billroth, 740. Binz, 727. Birch, 493. Bird, Golding, 539. Bitter-almond water in valvular diseases, 167. Bizot, 12, 189, 202, 364, 374, 550. Blache, 681, 685, 699, 702, 724. Blachez, 99. Black, 201, 963. Blaud, 681. Bleeding in subacute verrucose endocarditis, 93. Blennorrhoea, conjunctival, during dentition, 733. Blisters in treatment of valvular diseases, 167. Blix, 195. Blondeau, 843. Blood, increase in quantity of, in etiology of hyper- trophy of heart, 194. Blosfeld, 12. Bloxam, 452. Bochdalek, 474. Bodenheimer, 288, 659 Boerhave, 905. Boettcher, 254. 998 INDEX. Bollinger, 394, 779. Bonet, 534. Botkin, 135, 168. Botschetchkaroff, 170. Borellus, 274. Bouchard, 443. Bouchardat, 543. Bouchut, 724. Bouillaud, 19, 51, 62, 85, 90, 128, 209, 220, 226, 292, 363, 460, 54S, 556, 592, 604, 628, 630, 631, 632, 896. Bouvel-Roneiere, 518. Brain, affections of, in acute diphtheritic endocar- ditis, 69; in acute myocarditis, 235; in stenosis of the ostium aorticum, 145; in stenosis of the pulmonary ostium, 159; in subacute verrucose endocarditis, 89; in whooping-cough, 698, 699. Brain, diseases of, following chronic endarteritis, 384. Breidenbach, 728. Breschet, 687, 709, 796. Bretonneau, 827, 887, 958, 966. Bricheteau, 962. Broadbent, 117. Broca, 392, 408, Brodowski, 392. Bromide of ammonium in whooping-cough, 727; of potassium in whooping-cough, 727. Bronchitis in acute myocarditis, 235; in congenital diseases of the heart, 32S; in insufficiency of the mitral valve, 123; in stenosis of the pulmonary ostium, 158; in whooping-cough, 702. Broussais, 681. Brown, 756. Browne, R. K., 966. Bruberger, 216, 467. Bruckmiiller, 444. Brummerstaedt, 443. Brunniche, 723. Brims, 832, 834, a37, 843, 848. Bruzelius, 195. Bryant, 452. Buchanan. 527. Bucquoy, 482. Budd, 85. Budge, 277. Buhl, 106, %'&, 364, 928, 958. Buist, 555. Burchardt, 725. Burkhart, 66. Burns, Allan, 33, 151. Bnsch, 816. Butter, 680. van der Byl, 199, 296. Caffeine in acute myocarditis, 239 Calomel in whooping-cough, 727. Calvert, 963. Camphor in acute diphtheritis endocarditis, 81; in noma, 816 ; in whooping-cough, 727. Cancer in etiology of atrophy, 221. Canstatt, 681, 813, 857. Cantharides in treatment of chyluria, 543. Capillary systems, interference with, in etiology of hypertrophy of heart, 192, 197. Carbolic acid in stomatitis catarrhalis, 769. Carbonate of ammonia in acute diphtheritic endocar- ditis, 81; in treatment of heart clots, 297; of potassa in thrush, 806; in valvular diseases, 169; of soda in thrush, 806; inhalation of, in subacute verrucose endocarditis, 93. Carnochan, 276. Carter, 539. Castor in whooping-cough, 727. Catiano, 453. Cathartics in whooping-cough, 721. Cautery, actual, in noma, 817. Cejka, 583, 591, 595. Celsus, 268. Cerf, E., 630, 631. Chambers, 100, 552, 556, 630, 632,659. Charcoal in noma, 816. Charcot, 78, 443, 478. Chauveau, 16, 53, 59, 63. Cherry-laurel water in valvular diseases, 167. Chestnut, extract of, in whooping-cough, 727. Cheselden, 632. Cheston, Browne, 520. Chevers, 12. Chiene, 478. Childbirth in etiology of subacute verrucose endocar- ditis, 86. Chinoidine in whooping-cough, 726. Chisholm, 292. Chloral in valvular diseases, 171; in whooping- cough, 721. Chlorate of potassa in noma, 816; in stomatitis catarrhalis, 769; in prophylaxis of mercurial stomatitis, 790. Chloride of iron in noma, 816; of sodium in noma, 816. Chloroform in nervous palpitation, 307. Chlorosis in etiology of atrophy, 221. Chomel, 458. Church, 413. Cicatrix after wounds of heart, 282. Cicuta in whooping-cough, 726. Ciniselli, 456. Clar, 723. Clarke, 252. Clendinning, 12, 203. j Climate in etiology of whooping-cough, 683 ; in treat- 1 ment of valvular diseases, 166. INDEX. 999 Cloetta, 205. Cobbold, 542. Cochineal in whooping-cough, 727, Cockle, 452. Coester, 509. Cohen, 112. Conn, 477. Cohnheim, 67, 104. Cold in acute diphtheritic endocarditis, 80 ; in acute myocarditis, 238; in aneurism, 461; in exarteri- tis, 348; in glossitis, 750; in hypertrophy of heart, 218; in nervous palpitation, 306; in peri- carditis, 618; in valvular disease"., 167; in wounds of the heart, 284. Coley, 528. Colles, 501. Collin, 548, 591, 592. Color of endocardium in acute diphtheritic endocar- ditis, 65. Combean, 844. Commenge, 724. Compression in aneurism, 452. Congestion, pulmonary, following heart disease, 106. Conium in whooping-cough, 726. Constant, 709. Cooper, Astley, 452, 459, 520, 521, 530. Coote, 289. Copaiba in chyluria, 543. Copland, 221, 681. Cornil, 364, 490. Corrigan, 53, 63, 136, 816. Corrosive sublimate in noma, 816; in stomatitis catarrhalis, 769. Corvisart, 62, 83, 99, 189, 195, 225, 261, 411, 413, 548, 556, 582. 603, 615, 622, 628, 635, 665. Cotton, J. Payne, 305. Cough in dilatation of heart, 213 ; in whooping-cough, 692, 694. Coulon, 959. Coulson, 976. Craigie, 226, 473, 858. Crefeld, 330. Crevaux, 540. Crisp, 410, 414, 435, 437, 443. Croton-chloral in valvular diseases, 171. Croupous laryngitis in whooping-cough, 702. Crowfoot, 482. Cruveilhier, 183, 292, 443, 522, 550. Cubitt, 539. Cullen, 721, 727. Cunningham, 542. Curran, Warring, 619, 963. Cyanosis in congenital diseases of the heart, 325; in dilatation of heart, 212; in insufficiency of the pulmonary valves, 155; of the tricuspii valve, 150 ; in pericardial adhesions, 636 ; in stenosis of the pulmonary ostium, 148. Cyon, 298. 300. Czerny, 409. Daly, 460. Danvin, 961. Danz, 680. Davaine, 289. Davidson, 376. Davies, Herbert, 92. Davis, Thomas, 271. Davis, Thomas D., 727. Debize, 841. Debout, 726. Deglutition in aneurism of aorta, 426, 434. Deguise, 271. Delaberge, 966. Delafond, 958. Demme, 227, 230, 233, 237, 945, 964. De Renzi, 401. Desault, (524. Disclaux, 569. Desjardin, 537. Desnos, 887. Desruelles, 681. Deutsch, 816. Devergue. 263. Dewar, 963. Diabetes in etiology of atrophy, 221. Diagnosis. See different diseases. Diaphoretics in valvular diseases, 169. Diarrhoea in acute diphtheritic endocarditis, 76. Dickinson, 376. Diesterweg, 107. Diet in aneurism, 459; in pericarditis, 618; in sub- acute verrucose endocarditis, 92. Dietrich, 226. Digestive system, affections of, in heart disease, 112 ; in whooping-cough, 707. Digitalis in acute diphtheritic endocarditis, 80; in hypertrophy of heart, 218; in nervous palpitation, 306; in pericarditis, 617; in valvular diseases, 167; in wounds of heart, 284. Dilatation of heart. See Hypertrophy. Dilatation and hypertrophy of heart following chronic endarteritis, 378. Dilatation of aorta in etiology of hypertrophy, 193; of pulmonary arterial system in etiology of hy- pertrophy, 197. Diphtheria of the skin, 948. Diphtheria in etiology of paralysis of the soft palate, 826. Dittrich, 106, 227, 241, 244, 312, 315. Diuretics in valvular diseases, 169. Diversus, Sal., 547. 1000 INDEX. Dogiel, 20. Dogney, 843. Donders, 14, 300, 389. Dorsch, 313. Drastics in valvular diseases. Dropsy in dilatation of heart, 212; in heart disease, 110 ; in insufficiency of the aortic valves, 140 ; of the pulmonary valves, 155; of the tricuspid valve, 150; in pericardial adhesions, 6^6; in stenosis of the pulmonary ostium, 159, Dressier, 658 Drosdorff, 170. Dubini, 2:0. Dunreuil, 204. Duchek, 63, 88, 100, 244, 248, 375, 413, 435, 438, 556, 582, 588, 615, 616, 633, 658, 667. Duchenne, 824. Ducrest, 195. Duncan, 281, 457, 681. Dnplay, 519. Dupuytren, 269, 362, 459, 530, 976. Durande, 276. Durante, 363. Durham, 452. Duroziez, 138, 376. von Dusch, 12, 63, 163, 192, 206, 315, 645. Dusol, 459. Dutoit, 453. Duval. 958. Dysentery in etiology of atrophy, 221. Dysphagia, in pericarditis, 603. Dyspnoea in acute myocarditis, 235; in aneurism of aorta, 425, 431; in congenital diseases of the heart, 327 ; in dilatation of heart, 212 ; in insuffi- ciency of the aortic valves, 140; in pericardial adhesions, 635; in pericarditis, 602; in stenosis of the ostium aorticum, 145; of the pulmonary ostium, 158. Ear, affections of, in parotitis, 837, 838; in whoop- ing-cough, 697, 706. Eberth, 958. Echinococci in etiology of spontaneous rupture, 262. Ecker, 317. Eckhard, 830. Eczema, a complication of difficult dentition, 775. Edgar, 809. Eggel, 539, 541. Eisenlohr, 66, 70, 659, 660. Eisenmann, 809. Electricity in bulbar paralysis of the tongue, 826 ; in nervous palpitation, 307. Elleaume, 263. Embolism in insufficiency of the mitral valve, 124; in subacute verrucose endocarditis, 89. Emetics in whooping-cough, 721. Emmert, 525, 858. Emminghaus, 526. Emphysema of lungs, influence of, upon position of the heart, 179; in whooping-cough, 698. Endarteritis in etiology of aneurism, 411. Endocarditis in etiology of acute myocarditis, 227. Endocardium, Diseases of the, 61. Bibliography, 61. History, 61. Acute Diphtheritic Endocarditis, Ulcerative Endocarditis, 64 ; bibliography, 64 ; pathology, 65; seat of the effusion, 65; parenchymatous changes, 65; affections of the spleen, liver, and kidneys, 69; the brain, 69; pericarditis and myo- carditis, 69; the lungs and the blood, 69; eti- ology, 70 ; symptomatology, 72; the typhoid form, 72; the pysemic form, 73; intermediate forms, 74; fever, 75; the pulse, 76; the digestive organs, 76; the nervous system, 77; diagnosis, 78; dura- tion, 79; prognosis, 80; treatment, 80. Acute and Subacute Verrucose Endocarditis, 81; bibliography, 81; pathological anatomy, 81; position of the lesions, 82; nature of the product, 83 , emboli, 84; etiology, 84 ; influence of rheuma- tism, 85; of age, 85; chidbirth and pregnancy, 86; old valvular diseases, 86; acute exanthema- tous diseases, 86; other diseases, 87; symptoma- tology, 87 ; general symptoms, 88 ; murmurs, 88; embolism, 89; diagnosis, 90; duration and re- sult, 91; prognosis, 91: treatment, 92. Contracting and Sclerotic Endocarditis, 93; bibliography, 93; pathology, 94; position of the lesions, 94; their mode of formation, 95; causes and frequency ofvalvular defects, 98; the effects of valvular defects in general, 100; pulmonary infarctions, 104; pulmonary congestion, 106; oedema of the lungs, 107; dyspnoea, 107; com- pression of left lung by hypertrophy of left ven- tricle, 107; compression of primary bronchus by dilatation of left auricle, 108; cyanosis, 108; oedema, 109; dropsy, 110; changes in the blood, 110 ; in the liver, 111; the stomach, spleen, and alimentary canal, 112; the kidneys and urine, 112; the nervous system, 115. Insufficiency of the Mitral Valve, 119; eti- ology, 119; pathology, 119; symptomatology, 120 ; results of percussion and auscultation, 121; the pulse, 123 ; course of the disease, 123 ; diag- nosis, 124; prognosis, 125. Stenosis of the Ostium Venosum Sinistrum, 125; pathology, 126; physical signs, 127; the pulse, 129; symptomatology, 130 ; diagnosis and prog?wsis. 131. Insufficiency of the Aortic Valves, 132; eti- ology, 132; pathology, 133 ; physical signs, 134 ; INDEX. 1001 the pulse, 136; symptomatology, 139; diagnosis, 140: prognosis, 141. Stenosis of the Ostium Aorticum, 142; patholo- gy, 142 ; physical signs, 143; the pulse, 144 ; symp- tomatology, 145; diagnosis, 145; prognosis, 146. Insufficiency of the Tricuspid Valve, 146; etiology and pathology, 147; physical signs, 148 ; the pulse, 149; symptomatology, diagnosis, and prognosis, 150. Stenosis of the Ostium Venosum Dextrum, 150; pathology, 150 ; physical signs, 151; symptoma- tology, diagnosis, and prognosis, 152. Insufficiency of the Pulmonary Valves, 153 ; etiology, 153 ; pathology, 153 ; physical signs, 154; symptomatology, 154 ; prognosis, 155. Stenosis of Ostium of the Pulmonary Artery, 155; etiology, 155; pathology, 156; physical signs, 157 ; symptomatology, 158; diagnosis, 160 ; p}~ognosis, 161. Combination of Various Valvular and Ostial Affections, 161. Treatment of Valvular Diseases, 164; prophy- laxis, 165 ; general hygienic rules, 166; local ap- plications, 167; internal remedies, 167. Engel, 203, 221. Epileptic fits in stenosis of the ostium aorticum, 145; of the pulmonary ostium, 159. Eppinger, 625. Ergot in whooping-cough, 727. Ergotine in cerebral aneurism, 443 ; hypodermic in- jection of, in treatment of aneurism, 453; internal use of, 460. Esmarch, 453. Etiology. See different diseases. Ettmuller, 680. Eulenburg, 298, 299, 729. Examination of heart, 21. Exanthemata in etiology of contracting and sclerotic endocarditis, 93; of fatty degeneration of heart, 250 ; acute complications of subacute verrucose, endocarditis, 86. Eye, affections of, in fatty degeneration of the heart, 256; in pericarditis, 603; in whooping-cough, 697, 706. Faber, 681, 688. Fallami, 727. Fallopius 268. Fantoni, 2a3. Farre. 330. Fatty degeneration in etiology of spontaneous rupture of heart, 261. Fauvel, 792. Fearn, 45. Feine, 659, 661. Ferber, A., 596, 699. Fergusson, 433. Fernelius, 225. Ferri chloridum in noma, 816. Fetscherin, 531. Fetzer, 528, 536. Fever in acute diphtheritic endocarditis, 75 ; in acute myocarditis, 235 ; in acute phlebitis, 488 ; in diffi- cult dentition, 776; in lymphangitis, 517; iu pericarditis, 571; in whooping-cough, 693, 694. Fieber, 723. Filaria sanguinis hominum, connection of the, with chyluria, 512. Fischer-Dietschy, 423. Fischer, G., 269, 272, 271, 280. Fluegel, 727. Foerster, 551, 660, S35. Fohmann, 530. Foot-and-mouth disease of cattle in etiology of sto- matitis ulcerosa, 779. Foramina, arterial, their situation, 9; venous, their situation, 9. Foreign bodies, introduction of into the sac in treat- ment of aneurism, 454. Forestus, 547. Forget, 145, 151, 201. Form of heart, changes in, 15. Forster, 185. Forster, 369, 632, 740, 962. Fraenckel, 201. Fraenkel, 962. Fraentzel, 195, 906. Frank, J., 681, 682, 658, 699, 813, 896. Frank, P., 751. Frerichs, 155, 510, 557, 852. Friedleben, 681, 687, 716. Friedreich, 22, 30, 33, 35, 36, 52, 56, 63, 81, 97, 108, 127, 147, 163, 193, 205, 2C6. 220, 254. 275, 317, 413, 552, 555, 5S5, 594, 600, 603, 618, 629, 633, 642, 044, 65S, 662, 668. Frin, 274. Frommolt, 100,130. Fuckel, 963. Fuller, 83, S5, 91. Gaetani, 529. Gairdner, 427, 630, 633. Galabin, A. L., 354, 378. Galen, 547. Gallerand, 681. Gallic acid in chyluria, 543. Galvano-puncture in aneurism, 455, Gamboge in valvular diseases, 169. Gangrene a result of chronic endarteritis, 383. Garrod, 853. Gastric ulcer following chronic endarteritis, 384. Gauster, 702. 1002 INDEX. Gay, J., 508. Geigel, 33, 35, 52, 128, 149, 216, 467. Geist, 630. Gelmo, 699. Gendrin, 8, 56, 128, 147, 181, 420, 435, 520, 548, 558, 569, 582, 591, 697, 615, 616, 632, 650, 680, 709. Genersich, 519. Genitals, diphtheria of, 948. Gent, 271. Gentian in valvular diseases, 168. Gerard, 272. Gerhard, 93, 112, 124, 162. Gerhardt, 47, 105, 203, 206, 296, 587, 588, 593, 594, 612, 661, 700. Ghisi, 827. Gibb, 716, 727. Girtanner, 680. Gimbert, 389. Gjorgevie, 527. Glands, lymphatic, affections of, in lymphangitis, 518. Glanders in etiology of acute myocarditis, 227. Gmelin, 853. Goldsmith, 963. Goll, 112. Goltz, 277, 298, 300. Gordon, 364. Gorup-Besanez, 666. Gout in etiology of chronic endarteritis, 375 ; of con- tracting and sclerotic endocarditis, 99; of phle- bitis, 488. Graeffner, W., 655. Grantham, J., 724. Graves, 86, 548, 659. Gravis, 843. Gregory, 317, 330. Greenhow, 412, 452. Griepenkerl, 727. Griesinger, 71, 116, 649. Grisolle, 749. Guarinoni, 547. Gubler, 86, 895, 966. Guersent, 681, 709, 966. Guibert, 681. Guibonrt, 541. Guiffart, 534. Gull, 350, 355. Giinsburg, 620, 630, 667, 966. Gusserow, 249. Gutbrod, 16. Guthrie, 966. Guttmann, 52, 298. Hache, 548, 615. Hismoptysis in stenosis of left ostium venosum, 130; ostium aorticum, 145. ] Haenisch, 170. Halbertsma, 156, 313. Haller, 547. Hallier, 800. Hammernik, 226, 380, 584, 5S6, 623. Harley, 543, 727. Hart, 550. Harvey, 15, 61, 261, 277, 375, 975. Hauke, 691, 723. Heart, Introduction to Diseases of the, 3 ; bibliography, 3; general anatomy of the heart, 7; changes of form and position, 13; origin of sounds of the heart, 18 ; methods of examination, 21; inspection, 21; palpation, 22 ; percussion, 23; auscultation, 25; physical symptoms oj dis- eases of the heart, 26 ; inspection, 26 : palpation, 37; the pulse, 41; percussion, 46 ; auscultation, 48; murmurs, 48; their endocardial and exocar- dial origin, 52 ; their differences and diagnosis, 54. Heart, Diseases of the, 175; Changes in Position, 175; bibliography, 175; classifica- tion, 176; normal position, 176; influence of age, 176 ; of inspiration, 177. Turning of the Heart on its Axis, 177. Changes in the Heart's Position dependent upon Gravitation, 178; influence of vesicular emphysema of the lungs, 179. Change of Position by Pressure, 181; pleuritic effusions, 181; pneumonia, 181 ; diseases of the mediastinum, 182; curvatures of the spine, 182 : abdominal diseases, 182; diaphragmatic hernia, 183. Changes in Position occasioned by Traction, 183; pathology, course, 184; diagnosis, 185; prognosis and treatment, 186. Hypertrophy and Dilatation, 187; bibliography, 187; history, 188; definition, 190 ; etiology. 191; the left ventricle, 191; narrowing of the aortic opening, 191; contraction of ascending aorta, 192; diminution in calibre throughout the whole arterial system, 192; interference with the capil- lary system, 192 ; sclerosis of arterial tracts, 193 ; dilatation of aorta and other vessels, 193 ; insuffi- ciency of aortic valve, 194 ; increase in the quan- tity of blood, 194; pathological changes in the heart, 194; question of idiopathic hypertrophy, 195 ; the right ventricle, 196; stenosis at origin of pulmonary artery, 196; narrowing of its calibre by pressure from without, 196; interference with capillary regions of the lungs, 197; clots in pul- monary artery, 197 ; over-distention of system of pulmonary artery, 197 ; hypertrophy of the au- ricles, 198 ; hypertrophy of the lohole heart, 198; etiology, 198; age and sex, 199; dilatation of the heart, 199; etiology, 199; increased pressure with- INDEX. 1003 in the cavity, or disease of the heart substance, 199; pathology, 202 : normal measurements of heart, 202 ; weight, 203 ; amount of enlargement, 203; changes of shape and position, 204; the tex- ture and color, 204; site of dilatation, 204 ; general view of etiology of hypertrophy, 204 ; symptoma- to'ogy, 205; the heart impulse, 206; percussion, 207; auscultation, 209; changes in the circula- tion, 210; the pulse, 210 ; general symptoms, 211; symptoms of dilatation, 212 ; percussion and auscultation, 212; disturbances in circulation, 212; dyspnoea, 212 ; symptoms of dilatation of right ventricle and right auricle, 213; diagnosis, 213; complications and sequelae, 216; course, ter- mination, and prognosis, 217; treatment, 218. Atrophy of the Heart, 219; history and etio- logy, 220 ; pathology, 221; symptomatology and diagnosis, 222; course, termination, prognosis, and treatment, 223. Myocarditis, 223; bibliography, 223; introduc- tion, 224; history, 225. Acute myocarditis, 226; etiology, 226; general description of the disease, 227; pathological anat- omy, 228 ; purulent inflammations, 229; abscess of the heart, 230; blood clots, 232 ; changes in the other organs, 232 ; symptomatology, 233; physical signs, 233; the pulse, 234; fever, 235; condition of skin, 235; brain symptoms, 235; the respira- tory organs, 235; the digestive organs. 235; di- agnosis, 236; course, duration, complications, and termination, 237; prognosis and treatment, 238. Chronic myocarditis, 239; etiology, 239; descrip- tion of the disease, 240; pathological anatomy, 240; the syphilitic form, 241: diagnosis, 242: course, complications, termination, prognosis, and treatment, 242. Aneurism, Partial, of Heart, 243; defini- tion, 243. Acute Partial Aneurism, 243; general descrip- tion, 243. Chronic Aneurism, 244; etiology, 244; site of the disease, 244; syphilitic myocarditis as a cause, 245; age and sex, 245; symptomatology, 245 ; diagnosis and prognosis, 246. Fatty Degeneration of the Heart, 246; bibli- ography, 246; introduction, 247; history, 248; etiology, 24S; general disturbances of nutrition, 248 ; disturbances which act locally, 250 ; chronic parenchymatous myocarditis, 252; influence of sex, 252 ; general description of the disease, 252 ; pathological anatomy, 252; symptomatology, 254 : physical signs. 255; brain symptoms, 256; diagnosis, 256; course, duration, termination, 257 ; treatment, 259. Spontaneous Rupture of the Heart, 259; bibli- ography, 259 ; introduction, 261; history, 261; etiology, 261; fatty degeneration, 261; myocar- ditis, 262 ; disease of coronary arteries, 202; new growths, gummy tumors, and echinococci, 262; other determining causes, 263; influence of sex and age, 263; pathological anatomy, 263; site of the rupture, 263 ; its characteristics, 264; symp- tomatology, 265 ; diagnosis, 266; prognosis, 266 ; treatment, 267. Wounds, Foreign Bodies of Heart, 267; bibli- ography, 267 ; history, 268; etiology, 269; gen- eral description of the disease, 271; pathological anatomy, 272 ; site of the injuries, 273; depth of wound, 274; the pericardium, 274; form and direction of wound, 274; the reparative pro- cesses, 274 ; symptomatology, 275 ; hemorrhage, 276; syncope, 276 ; the nervous system, 277; pain, 277; pulse, 278; physical signs, 278; diag- nosis, 278 ; complications and termination, 280; causes of death, 2S1 ; the cicatrix, 282 ; progno- sis and treatment, 283. New Growths and Parasites of the Heart, 284 ; bibliography, 284; history, 285; pathologi- cal anatomy, 286; fibromas, 286; formation of concretions, 286; lipomas, cysts, myomas, and car- cinomas, 287 ; tubercle, 288 ; parasites, 289 ; symptoms and course of the disease, 289 ; diag- nosis, 290. Heart Clots, 291; bibliography, 291; history, 292; etiology, 292; pathological anatomy, 294 ; symp- tomatology, 295 ; diagnosis, 296; prognosis, 296; treatment, 297. Nervous Palpitation of the Heart, 297; bibli- ography, 297; history, 298 ; etiology, 298; rela- tions of forces of innervation, 298; pathological anatomy, 303; symptomatology, 304 ; physical signs, 304; the pulse, 305 ; diagnosis, 305; course and prognosis, 306; treatment, 306. Congenital Diseases of the Heart, 311; bibli- ography, 311; history, 312; acardia and abnormal positions, 314 ; congenital narrowness and closure of the ostia of the right side of the heart, 314; pathology, 314; stenosis and atresia of the pul- monary artery with closure of the septum, 317 ; stenosis of the right conus arteriosus, with an opening in the interventricular septum, 319 ; sim- ple stenosis and atresia of the pulmonary artery, with an opening in the ventricular septum, 320; combined stenosis and atresia of the pulmonary artery, 322; analysis of cases of pulmonary sten- osis followed by tuberculosis of the lungs, 330; diagnosis, 338; prognosis, 340 ; treatment, 341. Heath, Christopher, 451. Heberden, 685. Hebra, 736. Heiberg, 66. 1004 INDEX. Heidenhain, S58. Heim, 628. Heine, 156, 303, 313. Heller, 525, 606. Helmstedter, 411, 484. Hemiplegia in subacute verrucose endocarditis, 89. Hemorrhages in whooping-cough, 697; in wounds of the heart, 276. Hemorrhoids. See Diseases of the Veins. Henke, 814. Henle, 368, 388, 829. Henoch, 727, 769 Hensen, 537. Hepp, 204, Herapath, 681. Herard, 69. Heredity in etiology of aneurism, 416. Herman, 850. Hermes, 816. Hertzka, 384. Hervieux, 699. Heschel, 286. Heubner, 367, 395, 396, 493. Heydenreich, 274. Heyfelder, 707. Heynsius, 53, 63. Hiffelsheim, 16. Hildenbrand, 814. Hinze, 832. Hippocrates, S08. Hirsch, 99, 684. 688, 783. Hirschfeld, 493. Hitzig, 457. Hodgkin, 551. Hodgson, 328. Hoegh, 459. Hoffmann, 534. Hoffmann, C. E. E., 375. Hoffmann. Fr., 680, 721. Hollerius, Jacob, 268. Holmes, 274, 452. Hope, 63, 151,181, 204, 226, 459, 615, 628, 630, 633, 639. Hoppe-Seyler, 534. Horn, E., 680. Housley, 294. Hubert, 560. Huefner, 658. Hueter, 630, 813, 958. Hufeland, 274, 680, 687, 721, 727. Hughes. Marshall, 531, 535. Hunt, 769, 816. Hunter, 315. Hutchinson, 442. Huxham, 292. Hydrarg. chlor. corrosiv. in noma, 816; in stomatitis catarrhalis, 769. Hydrarg. chlor. mitis in whooping-cough, 727. Hydrochloric acid in noma, 816. Hydrocyanic acid in nervous palpitation of heart, 307; in whooping-cough, 726. Hydrogen, peroxide of, in whooping-cough, 727. Hyoscyamus in whooping-cough, 720. Hypertrophy and dilatation of heart following chronic endarteritis, 378. Hypodermic injections of ergotine in aneurism, 453. Icterus in acute myocarditis, 235; in stenosis of left ostium venosum, Immermann, 479. Impetigo, a complication of difficult dentition, 775. Impulse of heart in dilatation, 212 ; in hypertrophy, 206. Infarctions, pulmonary, 101. Infection in whooping-cough, 688. Inhalations in whooping-cough, 723 ; of ozone in acute diphtheritic endocarditis, 81. Injections into the sac in aneurism, 454. Inspection in examination of heart, 21, 26. Insufficiency of aortic valve in etiology of hypertro- phy, 194. Iodide of potassium in aneurism, 460 ; in chyluria, 543 ; in general dilatation of the arteries, 404; in pericarditis, 619. Iodine in general dilatation of the arteries, 404. Ipecac in whooping-cough, 721. Iron in noma, 816; in pericarditis, 619 ; in valvular diseases, 167, 169; in verrucose endocarditis, 92. Isambert, 963. Issues in treatment of valvular diseases, 167. Jaccoud, 86, 364, 640. Jackson, Hugh lings, 117. Jacobsohn, 321. Jahn, 16, 681, 6S7. Jamieson, 448. Jansen, 389. Jennings, 431. Jobert, 278, 966. Jodin, 962. Johnson, 350, 354. Jones. 410. Jorg, 814. Juniper berries in valvular diseases, 169. Karmel, 768. 790. Keiller, 809, 816. Kennedy, 633. Kerchensteiner, 581, Kerkring, 292. Key, Axel, 4C9. Kidneys, affections of, in acute diphtheritic endocar- ditis, 69; in acute myocarditis, 236; in insuffi- INDEX. 1005 ciency of the aortic valves, 140; in pericarditis, ' 606 ; in subacute verrucose endocarditis, 87, 89 ; in valvular heart disease, 112; in etiology of chronic endarteritis, 376; of pericarditis, 557. Kimpen, 400. King, 108. Kipp, F.( 653. Kirkes, 72, 377, 558. Kiwisch, 53, 63. Kjellberg, 723. Klaatsch, 816. Klebs, 522, 958. Klob, 153, 179, 197, 230. Knight, 856. Knoll, Th., 42. Kobelt, 25. Kohler, 287, 626. Kolisko, 153. Kolliker, 15, 389. Kopp, 725. Kornitzer, 15. Koster, 351, 411, 522. Koster, W., 371. Kottmeier, 286. Krause, 194, 398. Krauspe, 403, 444. Kremnitz, 442. Kreyser, 481. Kreyssig, 62, 151, 225, 292, 628, 632. Kruckenberg, 681, 709. Kuchenmeister, 962. Kiirschner, 15. Kussmaul, 37, 45, 112, 313, 315, 317, 320, 322, 348, 478, 650, 784, 851. Kiittner, 391. Kiittlinger, 716. Kyber, 392, 588, 663, 622. Labadie-Lagrave, 87. Laborde, 726. Laennec, 38, 62, 82, 189, 209, 220, 225, 248, 292, 529, 548, 562, 622, 623, 628, 632, 635, 658. Lagauterie, 962. Lalor, 560. Lambl, 985. Lancereaux, 66, 76, 370, 395, 482. Lancisi, John Maria, 61, 189, 195, 248, 416, 635, 638. Landerer, 375. Landois, 40, 44, 63, 298, 299. Landry, 993. Lange, 816. Langenbeck, 453. Langhans, 352, 366, 367, 370, 371, 522, 535. Larcher, 195. Larrey, 209, 279, 281, 624. Latham, 226, 548, 616. Lawson, 415. Lead, acetate of, in aneurism, 459; in cerebral aneu- rism, 443. Lead-poisoning in etiology of chronic endarteritis, 375. Leared, 19, 99. Lebert, 85, 99, 161, 375, 413, 414, 416, 424, 439, 441, 448, 460, 556, 682. Lebert on congenital diseases of the heart, 311. Lecomte, 961. Lee, R., 205. Leeching in exarteritis, 348. Legroux, 413, 459 Lehmann, 853. Leitzen, 833. Lender, 81. L'Epine, 82. Lesser, 519, 537, 724. Letzerich, 682, 688, 711, 724, 958. Leudesdorf, 792. Leudet, 348, 556. Levin, 529. Levis, 455. Lewis, 393, 539, 541, 542. Leyden, 52, 200. Lichen, a complication of difficult dentition, 775. Lidell, 414. Liebreich, 171. Lieutaud, 628. Ligature in aneurism, 451, Lips and Cavity of the Mouth, Diseases of the, 733. Herpes Labialis, 733 ; bibliography, 733; defini- tion, 733; etiology, 734 ; pathological anatomy, 735; symptomatology, 736; treatment, 738. Hypertrophy of the Lips, 738; bibliography, 738; definition, 738; etiology, 739; symptom- atology, 739; diagnosis, 740 ; treatment, 741. Diseases of the Tongue ; anatomico-histo- logical observations, 741; the muscular ap- paratus, 742; vascular supply, 742; nerve sup- ply, 743 ; the mucous membrane, 743. Glossitis Parenchymatosa, 745; bibliography, 745 ; definition, 746; etiology, 746; pathological anatomy, 747 ; symptomatology, 748; diagnosis, 749; prognosis, 750; treatment, 750. Tumors of the Tongue, 751; bibliography, 751; etiology, 752; pathological anatomy, 752; symp- tomatology, 754; cancer, 754; diagnosis, 755; treatment, 756. Pathological Coatings of the Tongue, 757; bibliography, 757; the manner of protrusion, 757; form of the tongue, its surface and outlines, 758; color, thickness, and extent of the coat, 759; degree of moisture of the tongue, 760. Diseases of the Mucous Membrane of the Mouth, 762; bibliography, 762. 1006 INDEX. Stomatitis Catarrhalis, 762; definition, 762; etiology, 763 ; symptomatology and pathological anatomy, 764; course and progress, 766; treat- ment, 767; washes and gargles, 767; absorption of gargles, 768. Difficult Dentition, 770; formation of the milk-teeth, 770; symptomatology. 772; ulcera- tion, 772; increased secretion in mouth, 782; conjunctival blennorrhoea, 773; diarrhoeal com- plications, 773 ; cutaneous eruptions, 774 : ner- vous symptoms, 775; fever, 776. Stomatitis Ulcerosa, 777; bibliography, 777; stomatitis aphthosa, 778 ; etiology and pathogeny, 778; symptomatology, 779; diagnosis and treat- ment, 781; putrid sore-mouth, stomacace, stoma- titis mercurialis, 782; etiology, 782; pathology, 785; symptomatology, 785; diagnosis, 788; treatment, 789. Scorbutus of the Cavity of the Mouth, 791; bibliography, 791; etiology and pathogeny, 791 ; pathological anatomy, 793; symptomatology, 793 ; diagnosis and prognosis, 795; treatment,^'). Thrush, Fungus Formations in the Mouth, 797 ; bibliography, 797; etiology, 798; pathological anatomy, 800: the fungus, 801; symptoma- tology, 803; diagnosis, 805; prognosis, 806 ; treatment, 806. Gangrene of the Cheeks, Noma, bibliography, 807; etiology, 808; symptomatology. 810 ; patho- logical anatomy, 812 ; diagnosis, 813 ; treatment, 815. Neuroses of the Mouth, 817; bibliography, 817; sensory disturbances, 818 ; hypersesthesia, 818 ; anaesthesia, 819; anaesthesia of the nerves of taste, ageustia, 820 ; hyperaesthesia of the nerves of taste, hypergeustia, allotriogeustia, 821 ; treat- ment, 823 ; motor disturbances in the mouth, 823; general considerations, 823 ; protrusion of the tongue in unilateral paralysis, 824 ; bulbar paralysis of the tongue, 824; treatment, 826 ; diphtheritic paralysis of the soft palate, 826 ; eti- ology and pathogeny, 826; symptomatology, 827: diagnosis, prognosis, and treatment, 828. The Parotid Gland, 829; anatomico-physiologi- cal remarks, 829; parotitis, 830; bibliography, 830; etiology, 831; pathological anatomy, 835 ; catarrh of the ducts of the gland, 836; metas- tatic parotitis, 837 ; evacuations of the abscess, 837; complications, 838; symptomatology, 839; idiopathic parotitis, 839; swelling of the testicle, 842; deuteropathic or metastatic parotitis, 844; diagnosis and prognosis, 846; treatment, 847. Ptyalism. Salivatio, 849; bibliography, 849; etiology and pathogenesis, 850; symptomatology, 852; course, terminations, and prognosis. 854; treatment, 855. Deep Inflammation of the Connective Tissue of the Throat, Angina Ludovici, 857; bibli- ography, 857; etiology, 857 ; pathological anat- omy, 858; symptomatology, course, and termina- tions, 859; treatment, 860. Liver, affections of, in acute diphtheritic endocarditis, 69, 76; in chronic endarteritis, 385 ; in pericar- dial adhesions, 636; in whooping-cough, 707. Livingstone, 301. Lobstein, 375. Lochner, 723. Loebel, 226, 227, 245. Lombard, 693. Loomis, 444. Lorey, 726. Loschner, 681, 690, 716. Louis, 330, 548, 597, 615, 532. Lovage root in valvular diseases, 169. Lbvenson, 963. Lower, 638. Luce, 895. Ludwig, 16, 20, 112, 298, 353, 830, 850, 856, 857. Luken, 241, 286. Lungs, affections of, in acute diphtheritic endocar- ditis, 69 ; in acute myocarditis, 235; in hyper- trophy of left ventricle, 107; in insufficiency of the pulmonary valves, 154 ; in insufficiency of the mitral valve, 124 ; in insufficiency of the tricuspid valve, 150; in stenosis of the ostium aorticum, 145; in stenosis of the pulmonary ostium, 157 ; in whooping-cough, 698 ; following acute phlebitis, 489 ; influence of emphysema of, upon position of the heart, 179. Luschka, 8, 12, 63, 177, 286. Lusitanus, Jacutus, 547. Lymphatics, Diseases of the, 512; bibliog- raphy, 512 ; introduction, 512. Lymphangitis, Angioleucitis, 513; bibliography, 513; pathology, 514; etiology, 516; symptoma- tology, 517; prognosis, 518; treatment, 519. Degenerations, Neoplasms, 521; bibliography, 521; calcification, 521; cancer and tubercle, 521. Narrowing, Occlusion, and Dilatation, 523; bibliography, 523; etiology, 523 ; pathology, 525; symptomatology, 526; diagnosis and treatment, 528; narrowing and dilatation of the ductus thoracicus, 529; etiology, 529; symptomatology, 530; treatment, 531. Rupture of the Lymphatics, Lymphorrhagia, 532; bibliography, 532; rupture of the thoracic duct, 533; composition of the lymph, 536 : prog- nosis and treatment, 538 ; chyluria, 538 ; com- position, 538; etiology, 539; symptomatology, 540; nature of the disease, 541; the filaria sanguinis hominum, 542; treatment, 543. Lyons, 420. INDEX. 1007 Macall, 684, 685, 697, 702, 704, 706, 716. Maclean, 201. Macleod, 444. Magendie, 530, 811. Magnesia, sulphate of, in fatty degeneration of the heart, 259. Maier, 348. Maingault, 724. Maisch, 727. Maisonneuve, 752. Majer, K., 716. Malefern in chyluria, 543. Mannkopf, 155, 315. Marcus, A. Fr., 681. Marey, 14, 53, 63, 123, 130, 137, 144, 381, 423, 430. Marjohn, 815. Marvaud, 640. Mascagin, 520. Massa, 225. Mayer, 364, 958. Mayne, 548. McCullen, 680. McDowel, 659. McKendrick, 296. Meade, 364. Measles, a complication oi subacute verrucose endo- carditis, 86; in whooping-cough, 708. Measurements of heart, 202. Meckel, 192, 312, 370, 164. Meir, Rudolph, 71, 77. Mellin, 727. Meltzer, Fr. O., 680. Mental diseases, resulting from cardiac disease, 116. Mentone, climate of, in treatment of valvular dis- eases, 166. Mercury in exarteritis, 348; in whooping-cough, 727. Meschede, 498. Mettenheimer, 591. Meyer, H., 113, 156, 313, 317. Meyer, Joseph, 8. Mignot, 727. Millard, 946. Mineral acids in acute diphtheritic endocarditis, 80. Mineral waters in fatty degeneration of heart, 259; of Homberg, Kissingen, and Soden, in valvular diseases of heart, 168. Mitral valve, insufficiency and stenosis of, in etiology of atrophy, 221. Mittler, 746. Moinet, 195. Monneret, 86, 262, 895, 966. Monti, 723. Monro, 534, 535. Moore, 454. Morel-Lavallee, 659. Morgagni, 62, 225, 248, 261, 263, 269, 287, 292, 312, 458, 464, 481, 548, 022, 628, 635, 640. Morphine in nervous palpitation, 306; in pericarditis, 618; in valvular diseases, 171; in whooping- cough, 721; in wounds of heart, 284 Mosler, 830, 835, 848. Morton, 529, 531, 535. Mouth, diseases of. See Diseases of Lips and Cavity of Mouth Moxon, 452. Mueller, 959. Muhlig, 282. Muler, N., 268. Munck, 200. Munson, 534. Murchison, 115, 726. Murmurs in examination of heart, 48. Murray, 452. Muscles of soft palate, 868. Musk in whooping-cough, 727. de Mussy, Gueneau, 105, 375, 604. Myers, 99, 189, 195, 376, 414. Myocarditis in etiology of spontaneous rupture, 262. Narcotics in acute myocarditis, 239; in nervous palpitation, 306; in valvular diseases, 167; in wounds of heart, 284. Nasiloff, 958. Nasse, 116. Nationality, influence of, in etiology of whooping- cough, 684. Naunyn, 122. Nerves of soft palate, 870. Nervous system, affections of, in acute diphtheritic endocarditis, 77; in difficult dentition, 775; in fatty degeneration of heart, 256; in pericarditis, 603 ; in stenosis of the ostium aorticum, 145 ; in valvular heart disease, 115 ; in whooping-cough, 706; effects upon, by wounds of heart, 277. Neumann, 53, 905. Newman, 959. Nicholls, 262. Nicotine intoxication in etiology of contracting and sclerotic endocarditis, 99; in treatment of whoop- ing-cough, 726. Niemeyer, 206, 541, 721, 769, 858. Niemeyer, Paul, 54, 448. Nitrate of silver in noma, 816 ; in whooping-cough, 721, 727. Nitre in subacute verrucose endocarditis, 92. Nitric acid in noma, 816 ; in whooping-cough, 727. Nitrite of amyl in valvular diseases, 182. Nolet, 520. Nollet, 53. Norwood, 726. Nothnagel, 299, 361, 597. 1008 INDEX. Occupation in etiology of aneurism, 415. (Edema in heart disease, 109; of brain in whooping- cough, 698; of glottis in whooping-cough, 702 ; of lungs in acute myocarditis, 235 ; in insuffi- ciency of the mitral valve, 124 ; of lung, follow- ing heart disease, 107. Oedmansson, 493. Oehme, 539. Oertel, 827, 958. Oesterlen. 289, 290. Ogle, 117, 413, 441, 482, 896. Okes, 681. Oldham, 320. Olliver, 86, 478. Operative measures in pericarditis, 622. Oppolzer, 112, 237, 520, 524, 531, 662, 681, 690, 725. Ormerod, 248, 556. Orth, 106. Otto, 529. Ozanam, 706. Ozone, inhalation of, in acute diphtheritic endocar- ditis, 81. Paget, 248, 288, 488, 551. Pain in aneurism of thoracic aorta, 425; in insuffi- ciency of the aortic valves, 140; in parotitis, 840 ; in pericarditis, 604; in scorbutus, 793; in wounds of heart, 277. Palate, Soft Diseases of the, bibliography, 863; anatomical remarks, 863; the anterior sur- face of the soft palate, 864 ; the uvula, 865 ; pala- tine arches, 865; the tonsils, 866; the posterior surface of soft palate, 868; the muscular appa- ratus, 868; the vascular supply, 869; lymphatics, 869; nerves, 870 ; congenital variations in the soft palate, 871; general symptomatology, 872; inspection, 872; palpation. 873; motor disturb- ances, 874; difficulty in swallowing, 874 ; diffi- culty in the specific or modified movements of respiration, 875; difficulty in speech, 876; altered reflex movements, 876; sensory disturbances, 876 ; disturbances of objective sensitiveness to pressure and temperature, 876 ; disturbances of taste, 877; disturbances of ordinary sensation, 877 ; pain, 877; substances removed in diseases of the palate, 878; odors, 878; symptoms of spreading of affec- tions of the palate, 879; increase of mucus, 879 : cough and vomiting, 879; general treatment, 880; local applications, 880 ; general treatment, 881. Disturbances of Circulation, 882; anamia, 882; congestive hyperatmia, 883; passive hyper- emia, 884; hemorrhage, 884; mdema, 886. Inflammation of the Soft Palate, Anginas, 8S7; acute catarrhal inflammation, 889; etiology, 889; pathological anatomy, 890; symptomatology, 893; rheumatic angina, 895; the gouty form, 896; cachectic angina, 896; treatment, 896 ; chronic catarrhal inflammation, 897 ; etiology, 897; pathology and symptomatology, 898; treatment, 899; symptomatic catarrhal anginas, 900 ; angina of measles, 900; of rubeola, 901; of scarlatina, 901; of small-pox, 902; of erysipelas, 902; her- petic angina, 903; pemphigus, 905; treatment,%§; phlegmonous angina, 906; etiology, 906; pathol- ogy, 906; symptomatology, 908; diagnosis, 909 ; treatment, 910 ; inflammation of the tonsils, 911; etiology, 911; pathological differences, 911; symp- tomatology, 915 ; treatment, 920 ; anginas which regularly appear with stomatitis, 921; toxic angi- nas, 921; aphthous angina, 922 ; ulcerous angina, 922; angina mycotica, thrush of the palate, 923 ; croupous and diphtheritic anginas, 924; the de- posit, 926; pathological anatomy, 927; clinical considerations, 931; the milder forms, 932; the severe forms, 936 ; the gangrenous form, 945; diphtheria of the skin, 948 ; diphtheritic paral- yses, 950 ; scarlatinous diphtheritis, 950 ; of measles, 953; secondary diphtheritis, 953 ; non- specific pharyngeal diphtheritis, 954 ; etiology; 955 ; incubation. 959; treatment, 960. Gangrene of the Soft Palate, 964; etiology, 964; symptomatology, 965. Atrophy of the Palate and Especially of the Tonsils, 966 ; etiology, 967; pathology, 968. Hypertrophy of the Tonsils, 972; bibliog- raphy, 972; pathology, 972; etiology, 974 ; symp- tomatology, 974; treatment, 977. Syphilis of the Soft Palate, 978; erythema, 979; alteration of the epithelium, 979; papules and patches, 980 ; nodes, 981 ; ulcers, 981; cica- trices, 982; treatment, 984. Morbid Growths, 984; neoplasms of connective tissue and vessels, of fatty tissue, of muscles, 985 ; lymphatic morbid formations, 986 ; epithe- lial morbid formations, 988; cancer, 988; cysts, 990. Nervous Affections of the Soft Palate, 990 ; motor disturbances, 990; sensory disturbances, 993; disturbances of nutrition, 994. Paldamus, 681, 725. Palpitation in Pericardial adhesions, 638. Paracentesis pericardii, 622. Parasites in the lumen of arteries, 393. Parasites of the heart. See New Growths. Pare, Ambroise, 272. Parotid gland, diseases of the. See Diseases of Lips and Mouth. Paschutin, 519. Pasta, 292. Paterson, 523. Pau, climate of, in treatment of valvular diseases, 166. IND EX. 1009 Paul, 797. Peacock, 12, 189, 201, 313, 316, 320, 321, 4R3, 484, 630. Pearce, 722. Pelletan, 444. Pelvet, 244, 488. Penzold, 124. Percussion in acute myocarditis, 233 ; in aneurism of aorta, 418, 429, 432, 433 ; in chronic endarteritis, 378; in congenital diseases of the heart, 328; in dilatation of heart, 212 ; in examination of heart, 23, 40 ; in fatty degeneration of heart, 255 ; in hypertrophy of heart, 2U7; in insufficiency of the mitral valve, 121; of the aortic valves, 134; of the pulmonary valves, 154; of the tricuspid valve, 148; in nervous palpitation, 304 ; in steno- sis of the ostium aorticum, 143; of the pulmon- ary ostium, 157; of the left ostium venosum, 127; of the right ostium venosum, 151 ; in whooping-cough, 696; in wounds of heart, 278. Pericardial effusion in etiology of atrophy of heart, 221. Pericarditis in etiology of acute myocarditis, 227; of fatty degeneration of heart, 250. Pericardium, Diseases of the, 547; history, 547. Absence of the Pericardium, 549; bibliography and remarks, 549. Formation of Diverticuli, 549 ; bibliography and remarks, 550. Tendinous Spots (Milk Spots), 550; bibliog- raphy, 550; pathology, 551. Inflammation of the Pericardium, 552; bib'i- ography, 552; pathogenesis and etiology, 554 : di- visions of the disease, 555; its rarity as a pri- mary affection, 555; the secondary form, 556; influence of rheumatism, 556 ; time of occurrence of the heart affection, 557 ; influence of kidney affections, 557 ; of pyaemia, 558 ; its occurrence in the course of other diseases, 538; its frequency, 560 ; influence of age and sex, 560; pathological anatomy, 561; stage of hyperaemia, 561 ; the fibrinous exudation, 561; its characteristics, 502 ; quantity of the fluid exudation, 562; its character- istics, 563; formation of pus, 564; methods of prog- ress towards cure, 505 ; transition into chronic inflammation, 566; character of the effusion, 567; circumscribed form, 567; changes in the muscular structure of the heart, 567; fatty de- generation, 568; other pathological changes, 569; symptomatology, 570 ; subjective symptoms, 570 ; the fever, 571 ; physical signs, 571 ; friction sounds, 571; cardiac dulness and the apex beat, 571; grades of intensity of the disease, 572; the hemorrhagic form, 578; chronic forms, 579; the affection in children, 5S1; inspection, 581; palpa- tion, 583; percussion, 5S5; the pericardial fric- VOL. VI.—64 tion sound, 591; endocardial murmurs, 595; the pulse, 590 ; pressure of the effusion, 597; dis- turbances in the venous circulation, 599; the heart's cavities. 600 ; the respiration, 6 1; dysp- noea, 602 : dysphagia, 603; nervous symptoms, 603; affections of the eye, 603; pain, 604; con- dition of the urine, 605; diagnosis, 607 ; charac- ter of the exudation, 607 ; the physical signs, 608; course, terminations, and prognosis, 612; treat- ment, 617; digitalis, 617 ; ice over the heart, 618 ; use of morphine and chloral, 618; diet, 618; diu- retics, 619; diaphoretics. 619 ; after-tieatment and treatment of complications, 620; treatment by operation, 622. Tuberculab Pericarditis, 624 ; pathology, symp- tomatology, diagnosis, and treatment, 625. Carcinomatous Pericarditis, 626; pathology and symptomatology, 626. Adhesions between the Heart and Pericar- dium 627 ; bibliography, 627 ; history, 628 ; etiol- ogy, 629; pathology, 631 ; general description of the disease, 635; analysis of individual symp- toms, 638; palpitation, 638; hypertrophy, 638 ; valvular insufficiencies, 640 ; absence of the apex- beat, 640 ; the cardiac dulness, 641; systolic de- pression in the place of the deficient apex-beat, 641; diastolic heart-beat, (545 ; diagnosis, 646 ; course and prognosis, 648 ; treatment, 649. Indurated Mediastino-pericarditis and Para- doxical Pulse, 649. Pneumopericardium, 657; bibliography, 657; eti- ology, 058; composition of the gas, 658: symp- tomatology, 660 ; diagnosis, 663: treatment, 6 >3. Hydropericardium, 661: bibliography. 664; com- position of the fluid, 665 ; etiology, 667; symp- tomatology, 668; diagnosis, 670 ; prognosis, 670 ; treatment, 671. HiEMOPERiCARDiuM, 671; etiology, 071; symptom- atology, 671. Free Bodies in the Pericardium, 672. Pericardium, puncture of, in hydropericardium, 671. Perl, 249, 492. Perls, 12. Permanganate of potassa in stomatitis catarrhalis, 769. Pertussis convulsiva. See Whooping-cough. Peruvian bark in whooping cough, 727. Pestalozzi, 44B. Peter, -Michel, 140, 844, 946, 958. Petit, 292. Petrequin, 455. Petters, 524, 530, 531. Pfeufer, 709. Philipp, 582. Phosphorus poisoning in etiology of fatty degenera- tion, 250. 1010 INDEX. Phthisis following whooping-cough, 705. Physical symptoms of diseases of the heart. Piorry, 63,628. Pirogoff, 8. Pisa, climate of, in valvular diseases. Pissinius, Sebastian, 292. Pitcairn. 556. Pitha, 966, 976. des Planches, Tanquerel, 854. Pleischl, 591. Plessimeter in examination of heart, 23. Pleura, affections of, in whooping-cough, 693, 705. Pleurisy in etiology of acute myocarditis, 227. Pneumatic treatment in valvular diseases, 170. Pneumonia in whooping-cough, 703 ; in etiology of acute myocarditis, 227. Podrazky, 279. Poiseuille, 53. Polotebnow, 193, 372. Ponfick, 116, 249, 250, 251, 391, 413, 439, 481. Porter, 444. Position and anatomy of the heart, 7. Position, change of, of heart, 13; of the body, in- fluence of, in inspection of heart impulse, 22. Potain, 51, 623. Potash, acetate of, in pericarditis, 618 ; in valvular diseases, 169; bromide of, in whooping-cough, 727 ; carbonate of, in thrush, 806: in valvular diseases, 169; chlorate of, in noma, 816 ; in stoma- titis catarrhalis, 769 ; in prophylaxis of mercurial stomatitis, 790; iodide of, in aneurism, 460 ; in chyluria, 543; in general dilatation of the arteries, 404; in pericarditis, 619 ; permanganate of, in stomatitis catarrhalis, 769. Potassae et antimonii tartras in hypertrophy, 219. Pregnancy in etiology contracting and sclerotic en- docarditis, 98; of subacute verrucose endocardi- tis, 86; pregnancy in, prognosis in insufficiency of the mitral valve, 125. Prognosis. See different diseases. Prout, 539. Prurigo, a complication of difficult dentition, 775. Puerperal processes in etiology of acute myocarditis, 227 ; in etiology of fatty degeneration of heart, 250. Pulmonary artery, affections of, in etiology of hyper- trophy, 196, 197. Pulmonary congestion following heart disease, 106. Pulmonary infarctions, 104. Pulmonary oedema following heart disease, 107. Pulsatilla in whooping-cough, 727. Pulse in acute diphtheritic endocarditis, 76; in acute myocarditis, 234; in aneurism of aorta, 422, 431 ; in chronic endarteritis, 380 ; in examination of heart, 41; in hypertrophy of heart, 210; in in- sufficiency of aortic valve, 130; of mitral valve, 123 ; of tricuspid valve, 149; in narrowing of the aorta, 475; in nervous palpitation, 305; in peri- cardial adhesions, 636; in pericarditis, 596; in stenosis of the ostium aorticum, 144; of the left ostium venosum, 129; in wounds of the heart, 278. Purgatives in aneurism, 459. Pyaemia in etiology of acute myocarditis, 227 ; of peri- carditis, 558; of phlebitis, 488; following exarter- itis, 348. Pyroligneous acid in noma, 816. Quain, 248, 261. Quassia in valvular diseases, 168. Quevenne, 540. Quincke on diseases of the vascular system, 345. Quinine in acute diphtheritic endocarditis, 80; in acute myocaiditis, 239; in chyluria, 543; in hy- pertrophy of heart, 219; in pericarditis, 619,622; in subacute verrucose endocarditis, 92; in valvu- lar diseases, 169; in whooping-cough, 721, 727. Race, influence of, in etiology of whooping-cough, 684. Ranvier, 364, 367, 371. Rauchfuss, 82. Ravoth, 501. Rayer, 541, 543, 854. von Recklinghausen, 68, 287, 2S9, 522. Rehn, 691, 722. Reiche, 752. Reisch, 34. Reitz, 958. Remak, 799. Reubold, 801. Requin, 749. Respiration in acute diphtheritic endocarditis, 75; in aneurism of aorta, 425, 432; in fatty degenera- tion of heart, 256; in pericarditis, 601. Rest in acute myocarditis, 238 ; in aneurism, 458. Rest-harrow root in valvular diseases, 169. Retina, pulsation in, in aneurism of aorta, 425, 432. Rey, 816. Rheumatic diseases in etiology of acute myocarditis, 227 ; of aneurism, 416; of chronic endarteritis, 375; of chronic myocarditis, 239; of contracting and sclerotic endocarditis, 98; of pericarditis, 556; of subacute verrucose endocarditis, 84. Rhubarb in stomatitis catarrhalis, 769; in valvular diseases, 168. Richardson, 93, 296, 729. Richter, A., 269, SOS. Ricord, 99, 241, 851. Rilliet, 85, 581, 630, 681, 685, 688, 700, 706, 713, 725, 813, 840, 960. Rindfleisch, 107, 205, 230, 241, 369, 474, 522, 564. Ringer, Sidney, 54, 727. iNDEr:. 1011 Riolan, 547, 622, 623. Robert, 976. Roberts, 539. Robin, 971. Rochard, 832. Roe. Hamilton, 681, 715. Roell, 779. Roever, 299. Roger, 117, 595, 698, 699, 723, 724, 828, 962. Rohrig, 530, 537. Rokitansky, 63, 192, 204, 211, 226, 244, 245, 248, 292, 294, 304, 312, 315, 317, 347, 351, 354, 370, 374. 370. 401, 411, 431. 443, 465, 474, 482, 522, 525, 530, 531, 535, 551, 568. Romero. 622. Rondolet, 547. Rosen, 727. Rosenstein, 193, 557, 680, 684. Rosenstein, introduction to diseases of the heart, 3; on diseases of the endocardium, 61. Rostan, 266. Rota, 325. Roth, 85, 193, 232. Rouanet, 19. Rouge, 453. Roux, 271. Ruckert, 400. Riidinger, 563. Rupture of aneurism of aorta, 427, 431, 433, 434, 438; in narrowing of the aorta, 476, Rupture, spontaneous, of heart. See Spontaneous Rupture. Rust, 816. Sakxinger, 659. Salesse, 543. Salicylate of soda in pericarditis, 620. Salicylic acid in treatment of diphtheritic endocarditis, 80. Sander, 69. Sanders, 628. Sandifort, 312. Sanson, 963. Sauvages, 680. Scammony in valvular diseases, 170. Scarification for removing oedema following valvular diseases, 170. Scarlatina a complication of subacute exanthematous endocarditis, 86. Scheele, 420. Scheiber, 204. Schenck, 680. Schiffer. Julius, 799. Schipmann, 323. Schlakon, 729. Schmidt, C, 798. Schnitzler, 76. Schott, 699. Schrock, L., 272. Schroetter on changes in the position of the heart and diseases of the heart substance, 175. Schuh, 622, 752. Schuler, 318. Schuppel, 493. Schutzenberger, 348, 640. Schwalbe, 453. Schwanda, 963. Schweigger Seidel, 11. Sclerosis of arterial tracts in etiology of hypertrophy, 193. Scrofula in etiology of stomatitis ulcerosa, 779. Scurvy in etiology of pericarditis, 578. Sea=on< in etiology of whooping cough, 684. Scbregondi, 698. Sedillot, 896. See. 117, 828. Segalas, 288. Seidlitz. 558, 563. Seitz, 99. 125, 189. 201, 376. Semilunar valve, its situation, 9. Seuac, 62, 188, 220, 225. 269, 292. 548, 5&3, 628. Sennert. 183. Sex in etiology of acute myocarditis, 227 ; of acute diphtheritic endocarditis, 72 , of aneurism, 415 , of cancer of the tongue, 752 : of chronic aneurism, 245 : of chronic endarteritis, 375 ; of chronic myo- carditis, 239; of congenital narrowing of the aorta, 465: of contracting and sclerotic endocar ditis, 100 ; of fatty degeneration of heart. 252, of hypertrophy of heart, 199, of pericarditis, 560: of spontaneous rupture of heart, 263; of whoop- ing-cough, 6S4 ; influence of, on frequency of ten- dinous spots on pericardium, 550 : in prognosis of insufficiency of the mitral valve, 125; of pericar- ditis, 616. Shaw, 976. Shelton, C. S 727. Siebert. S14, 816. Silver, nitrate of, in noma, 816; in vulvular diseases, I6S; in whooping-cough, 721, 727. Simon, S53. Simonet, 237. Size of heart, 11. Skin, affections of, in difficult dentition, 774. Skin, diphtheria of, 948. Skoda. 15, 19, 29, 55, 63, 123, 179, 182, 183, 206, 211, 226, 246, 304, 548, 593, 595, 600, 622, 629, 641, 658. Skrzecka. 253. Slavjansky, 358. Smith. 182. Smith. R. W., 413 Snow, 55s. 1012 IXDEX. Sobenheim, 226. Soboroff, 490. Soda, biborate of, in thrush, 806; carbonate of, in thrush, S06 ; inhalation of carbonate of, in suba- cute verrucose endocarditis, 93 ; salicylate of, in pericarditis, 620; sulphate of, in treatment of fatty degeneration, 259 , tartrates of, in subacute verrucose endocarditis, 92. Sodium, chloride of, in noma, 816. Soemmering, 550. Sounds of heart, origin of, 18. Speer, 155. Spengler, 348. Sperling, S2. Spleen, affections of, in acute diptheritic endocarditis, 69, 77; in pericardial adhesions, 636 ; in subacute verrucose endocarditis, 89. Sprengel, 0., 680. Squill in valvular diseases, 169. Stark, 201, 322. Steffen on whooping-cough, 675. Stehberger, 963. Steiermark, 858. Steiger. 660. Stein, 227, 228. 233, 234. 237, 257. Steiner, 118, 281, 685, 700, 726. Steveuart, 843. Stich, 482. Stimulants in acute myocarditis, 239 : in pericarditis, 621; in subacute verrucose endocarditis, 93. von Stoffela, 588. Stohr, 963. Stokes, 20, 63, 86, 185. 216, 226, 248. 255, 256, 409, 417, 430, 437, 449, 452, 458, 461, 548, 568, 572, 600, 65S. Stolker, 156. 158, 161, 327. Stoll, 690, 727, 896, 905. Stomach, affections of, in heart disease, 112. Stromeyer, 454, 747. Sucquet, 360. Sulphur in whooping cough, 727. Sulphuric acid in noma, 816. Sutton, 350, 355. van Swieten, 513, 622, 905. Symptomatology. See different diseases. Symptoms, physical, of diseases of the heart, 26. Syncope in wounds of heart, 276. Syphilis in etiology of acute myocarditis, 227; of cerebral aneurism, 441; of chronic endarteritis, 375 ; of chronic myocarditis, 239; of contracting and sclerotic myocarditis, 99; of fatty degenera- tion, 249 Talma, 19, 21, 135. Tanchon, 287. Tannin in aneurism, 459; in whooping cough, 727. Tartar emetic in hypertrophy, 219. Tartrates of soda in subacute verrucose endocarditis, 92. Taste in stomatitis catarrhalis, 765. Tea in acute myocarditis, 229; in dilatation of heart, 219. Teichmann, 528. Temperature of body in acute diphtheritic endocar- ditis, 75; in acute myocarditis, 235; in acute phlebitis, 48S; in difficult dentition, 776; in lymphangitis, 517; in pericarditis, 571; in steno- sis of the pulmonary ostium, 159; in whooping- cough, 093, 694. Testa. 292, 628, 638. Testicle, affection of, in parotitis, 842. Textor, 529. Thamra, 53. Thebesius, 287. Thiersch, 363, 752, 753. Thiry, 298. Thomas, 959. Thompson, 201, 659. Thompson, R. E., 555, 556. Thomson, 853. Thomer, 940. Thrombosis in etiology of acute myocarditis, 227 : in insufficiency of the mitral valve, 124. Thurn, 189, 195, 201. Thurnam, 245. Tiedemann, 478. Tissot, 263. Tobacco, use of, in etiology of cancer of tongue, 752. Tommasi, 479, 826, 958. Tongue, affections of, in whooping cough, 699. Tonics in subacute verrucose endocarditis, 92 ; in valvular diseases, 168. Tonsillitis in whooping-cough, 702. Tourdes, 808. Townsend. 289. Traube, 15, 18, 19, 20, 29, 42, 40, 63, 101, 114. 130, 134, 139, 143, 169, 192, 251, 371, 377, 587, 590, 598, 642, 654, 658. Travers, 330. Treadwell, 201. Treatment. See different diseases. Trocourt, 560. Trendelenburg, 958. Tricuspid valve, its situation, 9. Trideau, 964. Trousseau, 85, 622, 681, 692, 697, 703, 726, 627, 896, 958, 966. Tschudnowsky, 249. Tuberculosis in connection with congenital disease of the heart, 330. Tuberculosis in etiology of atrophy of heart, 221; in etiology of fatty degeneration, 249, INDEX. 1013 Tuckwcll, 117. Tuetel, 659. Tuffnell, 459. Tumors in etiology of spontaneous rupture, 262. Tiirck, 993. Turner, 903. Turpentine in noma, 816. Tussis convulsiva. See whooping-cough. Typhoid fever in etiology of fatty degeneration, 250. Typhus fever in etiology of atrophy, 221; in etiology of fatty degeneration, 250. Ulcer of stomach following chronic endarteritis, 3S1. Ur.gt. Hydrarg., in whooping-cough, 727. Ure, 853. Urine in acute myocarditis, 236; in pericardial ad- hesions, 636; in pericarditis, 605; in valvular heart disease, 112. Urticaria, a complication of difficult dentition, 774. Uterhart, 412. Valentine, 958. Valentiner, 254. Valerian in valvular diseases, 167; in whooping-cough, 727. Valerianate of zinc m whooping-cough, 727. Valleix, B., 805. Valsalva, 287, 458. Valve, aortic, insufficiency of, in etiology of hyper- trophy, 194. Valve, bicuspid, its situation, 9; semilunar, its situa tion, 9; tricuspid, its situation, 9. Valves of heart, affections of, following chronic en- darteritis, 379. Valvular disease of heart in etiology of subacute ver- rucose endocarditis, 86. Vanzetti, 459. Varicose condition of veins following chronic endar- teritis, 383 Vaslin, 964. Vast, 71. Van Veen, 155. Veins, Diseases of the, 486; bibliography, 486. Acute Phlebitis, 486; pathology, 486; etiology, 487; symptomatology, 488; treatment, 489. Chronic Phlebitis, 489; etiology, 489.pathology, 490; symptomatology, 490 ; treatment, 491. Hypertrophy, Atrophy, Degeneration, Neo- plasms of the Venous Coats, 491; general pa- thology, 491. Syphilitic Disease, 493; bibliography and path- ology, 493. Dilatation of the Veins, 494; bibliography, 494 ; pathology, 494; etiology, 495 ; symptoma- tology, 496 ; individual veins affected, 497; treat- ment, 500. Dilatation of the Hemorrhoidal Veins, 5U1; pathology, 501; etiology, 502, symptomatology. 504; diagnosis and prognosis, 506 ; treatment, 407. Narrowing and Obliteration, 508; etiology and pathology, 508. Rupture and Wounds, 509 ; etiology, 509 ; symp- tomatology, 510: prognosis and treatment, 511. Velpeau, 280, 354, 477, 520. Vena cava, its situation, 10. Venesection in wounds of heart, 284. Venous foramina, their situation, 9. Ventricle, left, its situation, 8. Veratrine in pericarditis, 619; in whooping-cough, 726. Veratrum viride in hypertrophy of heart, 218. Verney, 85, 90. Vernenil, 485. Vernon. G. Hannotte, 323. Vesalius, 62. Vesication in preventive treatment of subacute verru- cose endocarditis, 92. Vicrordt. 44. Vieussens, Raymond. 61, 548. 628, 635. 638. Virchow, 63, 65. 66, (K 69, 71, 86, 99, 106. 112, 192, 228, 250, 254, 2b5, 287, 294, 351, 304. 307, 369, 370, 371. 392, 394, 464, 465, 467, 469, 492, 519, 529, 560, 567. 568, 836, 8£8. Vogel. 85. Vogel on diseases of the lips and cavity of the mouth, 733. Voltolini, 978. Volz, 682. Vomiting in acute diphtheritic endocarditis, 76. Van de Vqorde, 808, 816. Voss, 322. Vulpian, 78. Wachsmuth, 606, 824. Wachtl, 727. Wade, 424. Wagner, 230, 248, 251, 254, 394, 522, 567, 6C6, 801. Wagner on diseases of the soft palate, 863. Wagstaffe, 286. Wahl, 153 Waldeyer, 2S9, 363. Wallmann, 481. Walshe, 28, 591, 659. Ward, 274. Warren, 976. Waters, mineral, in fatty degeneration of heart, 259 ; of Homburg, and Kissingen and Soden, in val- vular diseases, 168. Watson, Ebenezer, 722. )EX. i014 ixr Weber, 53, 63, 254, 420. Weber, A. 962. Weber, A. H„ 431. Weber, C. O., 364, 394, 443. 501 Weber, O., 230, 514, 533, 752, 7£3, 756. Webster, 681. Wedl, 373. Weight of heart, 11, 203. Weiland, 181. Weissmann, 205, Welch, 542. Wernher, 392, 518, 528, 860. Wertheimer, 959. West, 85, 684, 685, 693, 704, 706, 715, 723, 726, 769, 808, 946. Westphal, 77. Whipham, 65. Whitehead, 716. Whitley, 155, 315. Whitmarsh, 439. Whooping-cough, 675; bibliography, (Kb; his- tory, 679 ; definition, 682; mode of occurrence and causation, 683; geography, 683; climate, 684; seasons of year, 084; race and nationality. 684; sex, C84; age. 685; individual predisposi- tion, 686; immunity from the disease after one attack, 686; various theories as to causation of the disease, 0S6 : the author's theory, 688: in fection, 688: secretion of a specific virus in the air-passages, 689 ; mode of communication of the poison, 689; question of carrying the disease in clothing of non-infected persons, 689: other the- ories, 690; predisposing causes of attacks of coughing, 691; symptoms and course, 091; the prodromal stage, 692; cases of cessation of the disease at end of this stage, 693 ; the second, or spasmodic stage, 694; auscultation and percus- sion, 090 : duration and time of occurrence of the attacks, 697: hemorrhages, 697 ; affections of the brain, 698 ; the lungs and pleurse, 698; ulcera- tion of the tongue and frenulum, 699; duration of the spasmodic stage, 700 ; the stadium decre- menti, 700: its duration, 701 ; complications, 701; capillary bronchitis, 702 ; pneumonia, 703 ; atelectasis, 704; phthisis, 705; pleurisy, 705 . nervous symptoms, 706; the eye and ear, 706; the acute exanthemata, 707 ; pathological anato- my, 709; diagnosis, 712; prognosis, 715; treat- ment, 719 ;. prophylaxis, 720 ; internal remedies, 721; treatment during the attacks of coughing, 721; inhalations, 723 ; external remedies, 729. Wilkens, 15. Wilde, 684, 625. Wilks. 376, 395. 630, 647. Williams, 63, 248, 256, 420, 556. 629, 641, 9C6. Willigk, 199, 287, 560, 615, 625, 626. Willis, 680. Winckel, 493. Winge, 66. 70. Wintrich, 18, 56. Witsell, 717. Wolf, J., 208. Wolff, 63. Worbe, 264. Workmann, 99. Worms, 520. Wright, 853. Wrisberg, 520. Wulff, 13. Wunderlich, 85, 409, 685, G93. Winger. 971. Wutzer, 530, 750. Wyss, 564. Young, 816. Zahn, 487. Zaniboni, 722. Zdekaner, 457. Zehetmayer. 205, 585, 601. Zellner, 858. Zielonko, 205 Zimmermann, 350. Zinc, valerianate of, in whooping-cough, 727. * \ NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE SNmasw do Aavaan ivnoiivn snidiqsw do Aavaan ivnoiivn sNomaw do Aavaan ivnoiivn ^ -" x ISP i NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE NATIONAL LIBRARY OF MEDICINE * **\/ * \^$ ° j£*\./ 3NOia3w do Aavaan ivnoiivn snioicisw do Aavaan ivnoiivn snidicisw do Aavaan ivnoiivn ,4"x ° A^V ? 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